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Shaggy's Guide to Hormones used in Cannabis

shaggyballs

Active member
Veteran
A work in progress

As I study I post findings, so If you have something to add or find a mistake/error.... please post. The main reson we are here is to learn.

The use of growth regulators in agricultural production has increased due to their positive influence on
product quality.

With that said:
Remember to do your homework before using anything new!!!!!!!!!


Most of these phytohormones aren't properly tested on cannabis. Folks using it on their weed usually don't have much to do with toxicology testing or access to agriculture labs.


But don't kid yourself they are in every hydro store you walk in!!!!



As soon a plant sprouts it makes roots then try to producing more roots to acquire water/nutes.

Second they start building their leaf structure to acquire light.

Third the shoots start stretching and it tries to flower. The first two weeks are spent building things flowering requires. Once this is done it starts to produce flowering hormones.

But the flowering hormone is degraded by light. The plant builds up hormones all night and the sun comes along and kills them all. this cycle will repeat. Eventually days get shorter and nights get longer. More hormones are produced than the sun/light can kill. Each day more and more hormones survive the sun/light until they finally hit the right level and only then will flowering be induced.

It should be clarified that (most) hormones don't have a direct effect on plants. What plant hormones do is activate a signal cascade resulting in activation of genes which give response that is observed. Changes in concentration or usage of isomeric hormones has differing effects, thus the multiple effects seen from one hormone depending on the application method strength.

The effects of a hormone on a plant often depend on the stage of the plant's development.

Stages:

Clone,teen,veg,pre-flower,flower initiation,bud set,bulk up ect.

Plants progress through a cycle of growth stages. When a plant is under stress at any given stage of growth, it will produce less cytokinin growth hormones. If this reduction occurs at certain key stages of growth, yields are affected. By making available extra hormones to the plant at these stages, you can influence the plants final yield. Timing of the application is essential. If you apply a hormone to a plant, the result will be stimulated growth of the type which the plant is currently under going. If the plant is forming roots, more root growth will occur. These natural hormone compounds are essential to: plant cell enlargement and division - germination - root development - flowering and seed formation.

The correct usage of auxins and cytokinins used at varying ratios and times during the grow and flowering cycles can greatly stimulate desirable effects in plants. Auxins used in early grow, promote adventurous rooting, help relieve plant stress, and promote plant health/vigor.

Cytokinins, used during early bloom, can greatly aid in setting up a better plant structure (short squat plants with close internodes), and used thereafter can stimulate cell division (growth rates) and as a result increase yields.
All nutrients aside, balancing of the auxin/cytokinin/gibberellin chemical equation is the real key to maximizing your specific strains potential.
Mixing gibberellins with both auxins (IAA) and cytokinins (6BA) gives the treatment a synergizing balance and can exceed these limitations (i.e. a hardy ‘stretched out’ plant that is dense and full).

When the auxin concentration is lower than the cytokinin, explants will induce shoots, otherwise it will form roots.


That said the ratio, timing and type of hormones used will vary from stage to stage and is strain dependent.



Phytohormones: What Are they?

Plant growth and development involves the integration of many environmental and endogenous signals that, together with the intrinsic genetic program, determine plant form. Fundamental to this process are several growth regulators collectively called the plant hormones or phytohormones. This group includes auxin, cytokinin, the gibberellins (GAs), abscisic acid (ABA), ethylene, the brassinosteroids (BRs), and jasmonic acid (JA), each of which acts at low concentrations to regulate many aspects of plant growth and development. With the notable exception of the steroidal hormones of the BR group, plant hormones bear little resemblance to their animal counterparts. Rather, they are relatively simple, small molecules such as ethylene gas and indole-3-acetic acid (IAA), the primary auxin in the majority of plant species.

Phytohormones-Propagation pesentation
You may hit the slow or fast option if needed.

Agrobacterium tumefaciens bacteria

They produce and excrete auxin and cytokinin and it is possible that Salicylic acid and Jasmonic acid, which interfere with normal cell division and can cause largely undifferentiated calluses of cells.
 

shaggyballs

Active member
Veteran
Auxin

Auxins are plant hormones. The most important auxin produced by plants is indole-3-acetic acid (IAA).

It plays important roles in a number of plant activities, including:
development of the embryo
leaf formation
phototropism
gravitropism
apical dominance
fruit development
abscission
root initiation and development
the shade-avoidance effect
Embryonic Development

From the very first mitotic division of the zygote, gradients of auxin guide the patterning of the embryo into the parts that will become the organs of the plant:
shoot apex, primary leaves, cotyledon(s),stem, and root.
Link to illustrated description of seed development.

Leaf Formation

The formation of new leaves in the apical meristem [View] is initiated by the accumulation of auxin. Already-developing leaves deplete the surrounding cells of auxin so that the new leaves do not form too close to them. In this way, the characteristic pattern of leaves in the plant is established.

Auxin also controls the precise patterning of the epidermal cells of the developing leaf.

Phototropism

Plant shoots display positive phototropism: when illuminated from one direction, the shoot proceeds to grow in that direction.
Proposed Mechanism

The direction of light is detected at the tip of the shoot.
Blue light is most effective.
It is absorbed by a flavoprotein called phototropin. Flavoproteins contain flavin as a prosthetic group.
Auxin moves from the tip down.
An auxin transporter — one of the PIN proteins — is inserted in the plasma membrane at the lateral face of cells of the shoot.
Auxin is pumped out of these efflux transporters and accumulates in the cells on the shady side.
This stimulates elongation of the cells on the shady side causing the shoot to bend toward the light.
Link to some of the experiments that led to these conclusions.

Gravitropism

Gravitropism is a plant growth response to gravity.
Plant shoots display negative gravitropism: when placed on its side, a plant shoot will grow up
Roots display positive gravitropism: they grow down.
Possible Mechanism of Gravitropism in Roots

When a root is placed on its side,Statoliths (organelles containing starch grains) settle by gravity to the bottom of cells in the root tip.
This causes PIN proteins to redistribute to the underside of the cell where they pump auxin out of the cell; that is, they are efflux transporters.
The auxin then accumulates along the under side of the root.
This INHIBITS root cell elongation. [View reason for this.]
So the cells at the top surface of the root elongate, causing the root to grow down.
Apical Dominance


Growth of the shoot apex (terminal shoot) usually inhibits the development of the lateral buds on the stem beneath. This phenomenon is called apical dominance.

If the terminal shoot of a plant is removed, the inhibition is lifted, and lateral buds begin growth. Gardeners exploit this principle by pruning the terminal shoot of ornamental shrubs, etc. The release of apical dominance enables lateral branches to develop and the plant becomes bushier. The process usually must be repeated because one or two laterals will eventually outstrip the others and reimpose apical dominance.

Apical dominance seems to result from the downward transport of auxin produced in the apical meristem. In fact, if the apical meristem is removed and IAA applied to the stump, inhibition of the lateral buds is maintained.


The common white potato is really a portion of the underground stem of the potato plant. It has a terminal bud or "eye" and several lateral buds. After a long period of storage, the terminal bud usually sprouts but the other buds do not. However, if the potato is sliced into sections, one bud to a section, the lateral buds develop just as quickly as the terminal bud.


Fruit Development

Pollination of the flowers of angiosperms initiates the formation of seeds. As the seeds mature, they release auxin to the surrounding flower parts, which develop into the fruit that covers the seeds.

Some commercial growers deliberately initiate fruit development by applying auxin to the flowers. Not only does this ensure that all the flowers will "set" fruit, but it also maximizes the likelihood that all the fruits will be ready for harvest at the same time.

Abscission

Auxin also plays a role in the abscission of leaves and fruits. Young leaves and fruits produce auxin and so long as they do so, they remain attached to the stem. When the level of auxin declines, a special layer of cells — the abscission layer — forms at the base of the petiole or fruit stalk. Soon the petiole or fruit stalk breaks free at this point and the leaf or fruit falls to the ground.

The figure on the right shows a nice demonstration of the role of auxin in abscission. If the blade of the leaf is removed, as shown in the figure, the petiole remains attached to the stem for a few more days. The removal of the blade seems to be the trigger as an undamaged leaf at the same node of the stem remains on the plant much longer, in fact, the normal length of time. If, however, auxin is applied to the cut end of the petiole, abscission of the petiole is greatly delayed.

Fruit growers often apply auxin sprays to cut down the loss of fruit from premature dropping.


Root Initiation and Development

The localized accumulation of auxin in epidermal cells of the root initiates the formation of lateral or secondary roots.

Auxin also stimulates the formation of adventitious roots in many species. Adventitious roots grow from stems or leaves rather than from the regular root system of the plant.

Horticulturists may propagate desirable plants by cutting pieces of stem and placing them base down in moist soil. Eventually adventitious roots grow out at the base of the cutting. The process can often be hastened by treating the cuttings with a solution or powder containing a synthetic auxin.

Once a root is formed, a gradient of auxin concentration develops highest at the tip — promoting the production of new cells at the meristem, and lowest in the region of differentiation — promoting the elongation and differentiation of root cells. (The drop in auxin activity in the regions of elongation and differentiation is mediated by cytokinin — an auxin antagonist.)
Translocation of Auxin

Auxin moves through the plant by two mechanisms.

It passes in the sap moving through the phloem from where it is synthesized (its "source", usually the shoot) to a "sink" (e.g., the root).
It also passes from cell to cell by the following mechanism.

Auxin can enter the cell by diffusion and also through influx transporters in the plasma membrane. It moves out through efflux transporters — called PIN proteins. Eight different types of PIN proteins have been identified so far. These are transmembrane proteins inserted in localized portions of the plasma membrane, e.g., at the top of the cell where they move auxin toward the top of the plant;
at the basal surface of the cell where they move auxin down the plant;
at the lateral surface of the cell where they move auxin laterally (e.g., to mediate phototropism and gravitropism).
Identifying the signals that direct the appropriate placement of the PIN proteins is an active area of research.

How does auxin achieve its many different effects in the plant?

Auxin effects are mediated by two different pathways:
immediate, direct effects on the cell;
turning on of new patterns of gene expression
Direct effects of auxin

The arrival of auxin in the cytosol initiates such immediate responses as
changes in the concentration of and movement of ions in and out of the cell;
reduction in the redistribution of PIN proteins.
Some of the direct effects of auxin may be mediated by its binding to a cell-surface receptor designated ABP1 ("Auxin-binding protein 1").
Effects of auxin on gene expression

Many auxin effects are mediated by changes in the transcription of genes. The steps:
Auxin enters the nucleus and binds to its receptor, a protein called TIR1 ("transport inhibitor response protein 1") which now can bind to proteins responsible for attaching ubiquitin to one or another of several Aux/IAA proteins.
This triggers the destruction of the Aux/IAA proteins by proteasomes.
Aux/IAA proteins normally bind transcription factors called auxin response factors (ARF) preventing them from activating the promoters and other control sequences of genes that are turned on (or off) by auxin.
Destruction of the Aux/IAA proteins relieves this inhibition, and gene transcription begins.
This mechanism is another of the many cases in biology where a pathway is turned on by inhibiting the inhibitor of that pathway (a double-negative is a positive).

For example, the gibberellins, another group of plant hormones, exert their effects using a similar strategy. Link to a description.

The presence in the cell of many different Aux/IAA proteins (29 in Arabidopsis);
many different ARFs (23 in Arabidopsis), and several (~4) TIR1-like proteins provides a logical basis for mediating the different auxin effects that I have described. But how this is done remains to be discovered.


Synthetic auxins as weed killers

Some of the most widely-used weed killers are synthetic auxins. These include 2,4-dichlorophenoxy acetic acid (2,4-D) and 2,4,5-trichlorophenoxy acetic acid (2,4,5-T).

As the formulas show, 2,4,5-T is 2,4-D with a third chlorine atom, instead of a hydrogen atom, at the #5 position in the benzene ring (blue circles).

2,4-D and its many variants are popular because they are selective herbicides, killing broad-leaved plants but not grasses (no one knows the basis of this selectivity).

Why should a synthetic auxin kill the plant? It turns out that the auxin influx transporter works fine for 2,4-D, but that 2,4-D cannot leave the cell through the efflux transporters. Perhaps it is the resulting accumulation of 2,4-D within the cell that kills it.

A mixture of 2,4,-D and 2,4,5-T was the "agent orange" used by the U.S. military to defoliate the forest in parts of South Vietnam.

Because of health concerns, 2,4,5-T is no longer used in the U.S.
 

shaggyballs

Active member
Veteran
Key components in auxin perception and signalling. Auxin can modulate both transcriptional regulation and transcription-independent responses. In the nucleus, IAA binds to its receptors, the TRANSPORT INHIBITOR RESPONSE 1/AUXIN SIGNALLING F-BOX proteins (TIR1/AFBs) and to the auxin/indole-3-acetic acid (Aux/IAA) proteins. TIR1/AFBs are F-box proteins that form part of the SCFTIR1 complex, which consists of four subunits (TIR1/AFB, ASK1, CUL1 and RBX). An additional protein, RUB, binds to the SCFTIR1 complex to regulate its function. The TIR1/AFB and Aux/IAA proteins function as co-receptors for IAA, binding IAA with high affinity. When IAA levels are low (darker blue background), the Aux/IAA proteins form heterodimers with auxin response factors (ARFs) to repress gene transcription. The TOPLESS (TPL) protein functions as a transcriptional co-repressor for Aux/IAAs. However, when IAA levels are high, the binding of IAA to its co-receptors targets the Aux/IAA proteins for degradation by the 26S proteasome, which leads to derepression of ARF transcriptional regulation and the expression of auxin responsive genes. AUXIN BINDING PROTEIN 1 (ABP1), which is located in the endoplasmic reticulum (ER) or at the plasma membrane and/or in the apoplast (extracellular space), is also believed to function as an IAA receptor, mediating rapid auxin responses such as cell wall loosening, cytoskeleton rearrangement and regulation of endocytosis, leading to cell expansion.


The Speculative Overall Role is Oxygen deficiency signal.

Growth Direction Tendencies are Lengthening or elongating.

What is auxin's speculative complementary deficiency signal?
Ethylene!

If overall speculative role is true, what should auxin's affect be on synthesis?

Well-aerated plants should have high IAA levels, anoxia treated plants should have low levels. IAA should be mostly made in meristematic cells and much less so as cells mature. IAA should be made when a cell has more than enough oxygen to support both it any cell dependent on it for oxygen acquisition. Thus IAA is always an indication that growth amounts of oxygen are being procured by the plant and if conditions warrant, that the plant has enough oxygen to grow at least in the specific cell where the IAA is. (Shoot cells are responsible for acquiring oxygen for both it and some of the oxygen for a similar size cell in the root. Whereas a root cell is only responsible to itself for it own oxygen level and may even obtain some oxygen from spaces between soil particles).

If overall speculative role is true, what should auxin exogenous treatment produce?

Should induce ethylene, because IAA up regulates various processes limited by oxygen. Exogenously applying IAA leads the plant to falsely believe that it has high levels of oxygen, thus engaging all sorts of reactions that use O2, thus further depleting what may simply be a homeostatic level of existing O2 and moving this level into the deficiency range.

If overall speculative role is true, what should auxin inhibit and stimulate?

Should induces new root growth, just like JA. Especially if JA is also present, IAA should inhibit shoot growth because high JA and IAA levels are an indication of at least a short term lack of need to expand the shoots.

If overall speculative role is true, how should auxin affect storage?

Should cause O2 to be stored in proteins and sequestration methods for less propitious times.

If overall speculative role is true, how should auxin be transported?

May be expected to travel in the direction of the shoots, away the region lowest in O2, mainly the roots. As it travels up to the leaves it may actively send oxygen in the opposite direction.

If overall speculative role is true, how should auxin affect nutrient attraction and repulsion?

Should attract all nutrients and abundance hormones/signals to a cell and repel deficiency hormones/signals.

If overall speculative role is true, how should auxin affect apical dominance?

Should induce shoot apical dominance along with JA, however the possibility exists for two dominant apices if one is particularly good at sugar production (in the light) and one good at oxygen harvesting (in the wind). May break root apical dominances under conditions of low CK and SA.

If overall speculative role is true, how should auxin affect Cell Division?

Along with cytokinin and JA and Salicylic acid, IAA should be necessary for cell division. If there are some plant callus lines that will divide with only auxin and cytokinin present it is because these cell lines are mutants that produce SA and JA natively. Alternatively these latter two hormones are unknowingly being included with "other" nutrients/vitamins that are also added to calluses to get them to divide.

If overall speculative role is true, how should auxin affect Senescence

Should protect plant tissue from senescence, particularly root tissue.

If overall speculative role is true, how should SA effect growth directions to provide balance in the plant?

Auxin is known to generally lengthen plant parts, complementing it's deficiency partner, ethylene's broadening of plant parts.

Proven Synthesis and Transport

Made mostly in meristematic cells of the shoot and root decreasing as cells mature and age. 34 35 Why this makes sense - Under construction...

More is made in the shoot meristem than the root. 34 35 Why this makes sense - All the abundance signals are indications that certain meristems are worth sending nutrients to, e.g. investing in, and the strongest candidate in many species wins out to the exclusion of all others. Although possibly there is one dominant shoot apex for all four nutrient groups, water, minerals, sugar and gases making a total of four apices. Perhaps most of the time, the mineral and water apex and the sugar and gas apices are the same making two dominant apices, one for the root and one for the shoot.

Overall levels of auxin peak during the day. 36 Why this makes sense - like the other three abundance signals, excess "growable" amounts of nutrients, is more likely during the day when transpiration and photosynthesis are their peaks than at nights when nutrient stores are tapped to continue supporting life.

An internal gradient within the ovary effects the development of the of the embryo.
Why this makes sense - auxin appropriately induces new roots and cytokinin induces new shoots.
So if one end of the embryo is high in auxin, that end will become the root. If the other end is high cytokinin, that end will become the shoot.

The developing seed releases auxin, stimulating fruit growth. Why this makes sense - ?

Proven Effects

Auxin induces new adventitious root development and growth. 33 Why this makes sense - auxin induces new root growth to complement oxygen abundance. Since oxygen is mostly taken in by the leaves, abundance of it shifts growth away from the leaves to roots.

Involved in shoot and root phototropism. (The Cholodny-Went theory). Why this makes sense - ?
This doesn't make a lot of sense from the theory. Maybe phototropism is due to local relative paucity of oxygen because photosynthesis is using up O2. Therefore relatively speaking auxin will be higher in shaded sections of the root and shoot rather than that portion exposed to the sun. In the root the shaded excess of auxin leads to ethylene evolution and the relative inhibition of growth of the shaded section versus the one exposed to light.

May mediate positive root and negative shoot gravitropism.
Why this makes sense - perhaps the starch granules used to measure gravity are partly hydrolyzed and metabolized within the cells, leading to local oxygen depletion on the undersides of the cells in the roots and relative auxin abundance on the tops of the cells growing the cells down. In the shoots, the same thing happens but the relative

Induce xylem differentiation.
Why this makes sense - Opposite of what is expected, unless xylem somehow allows for oxygen transport down even though water at the same time is being transported up. However, maybe xylem differentiation may be to bring up water and minerals to complement the oxygen indicated by auxin and the sugar indicated by JA.

Auxin in concert with GA induce phloem differentiation.
Why this makes sense - this perhaps would make more sense if auxin were a sugar abundance signal. However an abundance of oxygen may be an indication of a lot photosynthesis having taken place, hence the need for removal of the sugar to where it's needed or stored.

Inhibits secondary buds below site of synthesis producing apical dominance.
Why this makes sense - perhaps success of the primary bud in terms of oxygen uptake and photosynthesis rates suggest against fooling with success and investing resources in new growth directions.

High levels of auxin induce ethylene synthesis especially in the roots.
Why this makes sense - since auxin is theorized to be an excess oxygen signal, perhaps it allows oxygen requiring processes such as metabolism to take place to such an extent that oxygen levels become depleted in the target tissue causing the release of the oxygen deficiency signal, ethylene.

Induce cell lengthening.
Why this makes sense - Cell lengthening requires processes require a lot of oxygen? Excess oxygen is sequestered in vacuoles, blowing a cell up like a balloon? complements ethylene's cell and tissue broadening.

An internal gradient within the ovary effects the development of the of the embryo.
Why this makes sense - as stated before, greater amounts of auxin would produce the root for the embryo whereas cytokinin would produce the shoot.

The developing seed releases auxin, stimulating fruit growth. Why this makes sense - ?
Young leaves strongly attract auxin preventing new leaves from growing out of the meristem too soon. 44 48 Why this makes sense - Maybe there is a "valley" where some amounts induce hibernation of leaf growth. Apical meristem growth is perhaps stimulated by the auxin it makes because it is beyond the valley of inhibition which is caused by moderate amounts of auxin.

When auxin are no longer produced by leaf, this initiates leaf senescence and abscission.
Why this makes sense - the roles of leaves is apparently primarily to make sugar with photosynthesis, to take in oxygen and carbon dioxide and to transpire. A leaf that is kept from senescence may need to do all four well or one more of the four extraordinarily well. Since apparently the four stimulating hormones attract each other if a leaf does not make auxin at all but only attracts it from neighboring supplies, a local synthesis may be necessary and so some oxygen uptake capabilities by a life may be necessary.

The Shade-Avoidance Effect.
Why this makes sense - this doesn't exactly make sense because the part of the plant exposed to sunlight would have the least amount of oxygen, since it is being used in photosynthesis. However if the location of where photosynthesis is transported to rather than where it is synthesized is important for auxin action then maybe the transport of auxin from the illuminated side to the dark side is what causes shade avoidance.

Auxin is integral to flower formation. Knockout auxin mutants do not flower.
Why this makes sense - ?
Auxin stimulates respiration. 113 Why this makes sense - increased auxin signals high oxygen thus allowing greater respiration.

Auxin changes carbon dioxide Levels in the Leaf.
Why this makes sense - increased respiration induced by auxin raises oxygen levels. Through this mechanism oxygen may regulate respiration and photosynthesis.
 

shaggyballs

Active member
Veteran
Cytokinins

Cytokinins are plant hormones that are derivatives of the purine adenine. (They are not to be confused with cytokines.)

They were discovered as an absolutely essential ingredient in medium for growing plant cells in culture. [View] Without cytokinins in the medium, plant cells will not divide by mitosis.

Cytokinins have been implicated in many plant activities; usually along with some other plant hormone such as auxin or ethylene.

Among these:
mitosis
chloroplast development
differentiation of the shoot meristem
stimulating the development of lateral buds and therefore branching
differentiation of the tissues of the root
leaf formation
leaf senescence

One of the clearest examples of cytokinin activity occurs in the germination of seeds. The endosperm of monocot seeds, such as corn (maize), contains large stores of the precursor to the cytokinin zeatin (right). When the corn kernel germinates, zeatin moves from the endosperm to the root tip where it stimulates vigorous mitosis.

The steps in cytokinin signaling:
A cytokinin, like zeatin, binds to a receptor protein embedded in the plasma membrane of the cell.
The internal portion of the receptor then attaches a phosphate group to a protein in the cytosol.
This protein moves into the nucleus where
it activates one or more nuclear transcription factors.
These bind to the promoters of genes.
Transcription of these genes produces mRNAs that move out into the cytosol.
Translation of these mRNAs produces the proteins that enable the cell to carry out its cytokine-induced function.



Speculative Overall Role

Root nutrition other than water abundance signal

Growth Direction Tendancies Broadening or widening
What is cytokinin's speculative
complementary deficiency signal?

Strigolactone

If overall speculative role is
true, where, when and which
cells should synthesize cytokinin?

Well fertilized plants should have high CK levels, plants living in poor soils should have low levels. CK should be mostly made in meristematic cells and much less so as cells mature. CK should be made when a cell has more than enough essential minerals to support both it any cell dependent on it for mineral acquisition. Thus CK is always an indication that growth amounts of minerals are being procured by the plant and if conditions warrant, that the plant has enough minerals to grow at least in the specific cell where the CK is. (Root cells are responsible for acquiring minerals for both it and similar size cells in the root. Conversely a shoot cell is only responsible to itself for it own mineral nutrition levels).

If overall speculative role is true, what
should exogenous cytokinin treatment produce?

Should induce strigolactones, because CK up regulates various processes limited by minerals. Exogenously applying CK leads the plant to falsely believe that it has high levels of minerals, thus engaging all sorts of reactions that use or are normally limited by mineral levels, thus further depleting what may simply be a homeostatic level of the existing fertilizers and moving this level into the deficiency range.

If overall speculative role is true, what
should cytokinin inhibit and stimulate?

Should induces new shoot growth, just like SA. Especially if SA is also present, CK should inhibit root growth because high SA and CK levels are an indication of at least a short term lack of need to expand the roots.

If overall speculative role is true,
how should cytokinin affect storage?

CK should cause excess minerals to be stored in vacuoles, storage proteins and tubers for less propitious times.

If overall speculative role is true,
how should cytokinin be transported?

CK may be expected to travel in the direction of the shoots, away from the roots and particularly away from root meristems. Regions of a cell or tissue or plant part that contains high CK, may particularly attract fertilizer type minerals and transport of important minerals may follow active or passive CK transport up a plant in the xylem or other tissue.

If overall speculative role is true, how should
cytokinin affect attraction and repulsion?

Should attract all nutrients and abundance hormones/signals to a cell and repel deficiency hormones/signals.

If overall speculative role is true, how
should cytokinin affect apical dominance?

Should induce root apical dominance along with SA, however the possibility exists for two dominant apices if one is particularly good at fertilizer absorption (in good soil) and one good at water harvesting (in the moist part of the soil). CK may break shoot apical dominances under conditions of low JA and IAA.

If overall speculative role is true, how
should cytokinin affect Cell Division?

Along with IAA and JA and Salicylic acid, CK should be necessary for cell division. If there are some plant callus lines that will divide with only auxin and cytokinin present, it is because these cell lines are mutants that produce SA and JA natively. Alternatively these latter two hormones are unknowingly being included with other nutrients/vitamins that are also added to calluses to get them to divide.

If overall speculative role is true, how
should cytokinin affect senescence?

Should protect plant tissue from senescence, particularly shoot tissue.

If overall speculative role is true,
how should cytokinin effect growth
directions to provide balance in the plant?

Cytokinin has been found to broaden plant parts, including leaves and stems. Should complementit's analogue deficiency signal strigolactones effect on plant growth. Strigolactones should lengthen plant cells and tissues.

Proven Synthesis and Transport

Made in high amounts in dividing shoot meristematic cells. 82 Why this makes sense - auxin and probably cytokinins, jasmonates and salicylic acid cause the the attraction of all nutrients to dividing cells including those in the shoot meristem. A high amount of minerals will exist then stimulate cytokinin synthesis which will attract even more minerals and other nutrients.

Made in the highest concentrations in the root meristematic cells. 83 Why this makes sense - roots will have the highest amount of minerals as of course this is where they first enter the plant.

Proven Effects

Exogenous CK inhibits senescence of leaves. 65 66 67 Why this makes sense - CK is an indication of excess or growth appropriate levels of minerals. These minerals need to be complemented by water, sugar and oxygen. Sugar and oxygen are made in the shoots, thus cytokinin acts to preserve them.

Induces new shoots in undifferentiated calluses. 115 Why this makes sense - See above.

Is integral to differentiation of the shoot meristem. 84 Why this makes sense - See above.

Stimulates the development of lateral buds and branching. 85 Why this makes sense - This is probably only true if there is a relative abundance of cytokinin over auxin and jasmonates indicating that the current shoot apical meristem directed growth is not meeting with the same success as the current root system. Thus the situation warrants other secondary meristems growing out and harvesting more auxin and making more sugar.

Induces cell broadening. 86 Why this makes sense - Cytokinin's broadening should complementit's deficiency signal partner strigolactones growth patterns which should be lengthening of plant parts.

Integral to root differentiation. 87 Why this makes sense - Cytokinin levels will determine presumably whether growth is strongly controlled by one root apical meristem like a Christmas tree or branching out.

Integral to leaf formation. 88 Why this makes sense - Should cause new leaves to be formed and should cause current ones to broaden catching more sunlight and harvesting more oxygen with both strategies.

Along with auxin, necessary to be present to induce cell division. 89 Why this makes sense - Unless there is a guaranteed surplus of minerals, oxygen, water and sugar, a plant knows it should not initiate new cells. Auxin and cytokinin would indicated the necessary amounts of minerals and oxygen. salicylic acid and jasmonate are probably also required before a plant starts a cell division.

Integral to chloroplast development 90 91 Why this makes sense - Again, minerals need to be complemented by water, oxygen, and sugar. Photosynthesis generates oxygen and sugar, so cytokinin is interested in maximizing this.





Cytokinins and root development

Gravitropism , development nitrate response, control of root meristem activity

Regulation of the root meristem activity by cytokinins

Cytokinin are essential for cell division, therefore very important for root meristem activity. Produced in root tip and vasculature of root mainly.
Altough essential for cell proliferation, cytokinin negatively regulate root meristem activity (exogenously supplied cytokinin inhibits root growth, and plant with a lower cytokinin content grow faster in plant overexpressing cytokinin oxidase (CKX) genes (The CKX proteins degrade irreversibly cytokinin).

Role of cytokinin in the regulation of root gravitropism

The models explaining root gravitropism propose that the growth response of plants to gravity is regulated by asymmetric distribution of auxin (indole-3-acetic acid, IAA). Since cytokinin has a negative regulatory role in root growth, Aloni et al (2004) suspected that it might function as an inhibitor of tropic root elongation during gravity response. Therefore, they examined the free-bioactive-cytokinin-dependent expression pattern in root tips , visualized high cytokinin concentrations in the root cap with specific monoclonal antibodies, and complemented the analyses by external application of cytokinin. Their findings show that mainly the statocytes of the cap produce cytokinin, which may contribute to the regulation of root gravitropism. The homogenous symmetric expression of the cytokinin-responsive promoter in vertical root caps rapidly changed within less than 30 min of gravistimulation into an asymmetrical activation pattern, visualized as a lateral, distinctly stained, concentrated spot on the new lower root side of the cap cells. This asymmetric cytokinin distribution obviously caused initiation of a downward curvature near the root apex during the early rapid phase of gravity response, by inhibiting elongation at the lower side and promoting growth at the upper side of the distal elongation zone closely behind the root cap. Exogenous cytokinin applied to vertical roots induced root bending towards the application site, confirming the suspected inhibitory effect of cytokinin in root gravitropism. Our results suggest that the early root graviresponse is controlled by cytokinin. They conclude that both cytokinin and auxin are key hormones that regulate root gravitropism.

Cytokinin and root response to nutrients

Cytokinin and nitrate, phosphate nutrition. Regulation of a set of phosphate starvation genes by cytokinins. Increase in cytokinin content in presence of nitrate. Regulation of Some AtIPT genes by nitrate

Cytokinins control key processes during plant growth and development, and cytokinin receptors

CYTOKININ RESPONSE
The involvement of cytokinins in signaling the status of several nutrients, such as sugar, nitrogen, sulfur, and phosphate (Pi), has also been highlighted, although the full physiological relevance of this role remains unclear. To gain further insights into this aspect of cytokinin action, we characterized a mutant with reduced sensitivity to cytokinin repression of a Pi starvation-responsive reporter gene and show it corresponds to AHK3. As expected, ahk3 displayed reduced responsiveness to cytokinin in callus proliferation and plant growth assays. In addition, ahk3 showed reduced cytokinin repression of several Pi starvation-responsive genes and increased sucrose sensitivity. These effects of the ahk3 mutation were especially evident in combination with the cre1 mutation, indicating partial functional redundancy between these receptors.We examined the effect of these mutations on Pi-starvation responses and found that the double mutant is not significantly affected in long-distance systemic repression of these responses. Remarkably, we found that expression of many Pi-responsive genes is stimulated by sucrose in shoots and to a lesser extent in roots, and the sugar effect in shoots of Pi-starved plants was particularly enhanced in the cre1 ahk3 double mutant. Altogether, these results indicate the existence of multidirectional cross regulation between cytokinin, sugar, and Pi-starvation signaling, thus underlining the role of cytokinin signaling in nutrient sensing and the relative importance of Pi-starvation signaling in the control of plant metabolism and development.

Nature of Cytokinins

Cytokinins are compounds with a structure resembling adenine which promote cell division and have other similar functions to kinetin. Kinetin was the first cytokinin discovered and so named because of the compounds ability to promote cytokinesis (cell division). Though it is a natural compound, It is not made in plants, and is therefore usually considered a "synthetic" cytokinin (meaning that the hormone is synthesized somewhere other than in a plant). The most common form of naturally occurring cytokinin in plants today is called zeatin which was isolated from corn

Cytokinins have been found in almost all higher plants as well as mosses, fungi, bacteria, and also in tRNA of many prokaryotes and eukaryotes. Today there are more than 200 natural and synthetic cytokinins combined. Cytokinin concentrations are highest in meristematic regions and areas of continuous growth potential such as roots, young leaves, developing fruits, and seeds.

History of Cytokinins

In 1913, Gottlieb Haberlandt discovered that a compound found in phloem had the ability to stimulate cell division (Haberlandt, 1913). In 1941, Johannes van Overbeek discovered that the milky endosperm from coconut also had this ability. He also showed that various other plant species had compounds which stimulated cell division (van Overbeek, 1941). In 1954, Jablonski and Skoog extended the work of Haberlandt showing that vascular tissues contained compounds which promote cell division (Jablonski and Skoog, 1954). The first cytokinin was isolated from herring sperm in 1955 by Miller and his associates (Miller et al., 1955). This compound was named kinetin because of its ability to promote cytokinesis. Hall and deRopp reported that kinetin could be formed from DNA degradation products in 1955 (Hall and deRopp, 1955). The first naturally occurring cytokinin was isolated from corn in 1961 by Miller (Miller, 1961). It was later called zeatin. Almost simultaneous with Miller Letham published a report on zeatin as a factor inducing cell division and later described its chemical properties (Letham, 1963). It is Miller and Letham that are credited with the simultaneous discovery of zeatin. Since that time, many more naturally occurring cytokinins have been isolated and the compound is ubiquitous to all plant species in one form or another (Arteca, 1996; Salisbury and Ross, 1992).

Biosynthesis and Metabolism of Cytokinins

Cytokinin is generally found in higher concentrations in meristematic regions and growing tissues. They are believed to be synthesized in the roots and translocated via the xylem to shoots. Cytokinin biosynthesis happens through the biochemical modification of adenine. The process by which they are synthesized is as follows (McGaw, 1995; Salisbury and Ross, 1992):
A product of the mevalonate pathway called isopentyl pyrophosphate is isomerized.
This isomer can then react with adenosine monophosphate with the aid of an enzyme called isopentenyl AMP synthase.
The result is isopentenyl adenosine-5'-phosphate (isopentenyl AMP).
This product can then be converted to isopentenyl adenosine by removal of the phosphate by a phosphatase and further converted to isopentenyl adenine by removal of the ribose group.
Isopentenyl adenine can be converted to the three major forms of naturally occurring cytokinins.
Other pathways or slight alterations of this one probably lead to the other forms.
Degradation of cytokinins occurs largely due to the enzyme cytokinin oxidase. This enzyme removes the side chain and releases adenine. Derivitives can also be made but the pathways are more complex and poorly understood.

Cytokinin Functions

A list of some of the known physiological effects caused by cytokinins are listed below. The response will vary depending on the type of cytokinin and plant species (Davies, 1995; Mauseth, 1991; Raven, 1992; Salisbury and Ross, 1992).

Stimulates cell division.
Stimulates morphogenesis (shoot initiation/bud formation) in tissue culture.
Stimulates the growth of lateral buds-release of apical dominance.
Stimulates leaf expansion resulting from cell enlargement.
May enhance stomatal opening in some species.
Promotes the conversion of etioplasts into chloroplasts via stimulation of chlorophyll synthesis.
 

shaggyballs

Active member
Veteran
My best guess at how to use cytokinins effectively!

cytokinins used at high ppm during cloning will prevent callus from forming roots and tell the plant to make shoots.
I have seen this myself.
I had shoots growing in a easy cloner with a constant spray of extremely weak clonex liquid on the roots.
I don't recommend cytokinins for clones!

You need to start low with just established clones.
Cytokinins inhibit downward root growth.
As high levels of cytokinins inhibit root growth in cannabis.
At the correct levels it will encourage lateral root growth while allowing for normal root length.(tiny root hairs)
As they get bigger you give them small doses at a time but slowly increase the ppm in soil or in REZ.
That is if you are looking to optimize root growth.

But remember this is strain subjective.
Shorter plants need less so as to maintain fast growth while stretchier strains need more to slow growth just enough!

If you want to change the shape of the plant(shorten it) then higher PPM is required.

Then wait 5-7 days so you give the plant a chance to react.
I apply small amounts in the rez. and then use frequent foliar sprays.
I you use a spray wait a few days if you don't like the results you can spray low doses more often to get the effect you are looking for.

Bud cycle is another story I am still lost here.
At the right time and PPM it will give you faster bud set!
I know if you don't get the timing right and you get the ppm's too high it will stop vertical growth and decrease yield especially when the plants have been topped!

These instructions are for using cytokinins by themselves.
I personally think they work better in a synergistic manner with auxin and brassinoloid,but then PPM must be recalculated.

Disclaimer
covers entire post
USUALLY


Types of Cytokinin

Ba 6 Benzylaminopurine-BAP

Is a first-generation synthetic cytokine.
Elicits plant growth and development responses.
Can force the plant into setting blossoms or budnodes.
Ba 6 Benzylaminopurine can stimulate fruit richness by stimulating cell division.
Is an inhibitor of respiratory kinase in plants.
Increases post-harvest life of green vegetables.
Promotes cell elongation and division in plants.
Regulates differentiation in tissue culture.
Ba 6 Benzylaminopurine can decrease the chances of flower dropping and fruit dropping.
Ba 6 Benzylaminopurine improves the plant's ability to deal with diseases.
Improves the growth of the germinating seed.
Can be used in drench or foliar feed applications.
Strengthens a plant's immunity to stresses such as drought, salinity and cold.
Is an important element for plant growth and helps increase yield.

Ba 6 Benzylaminopurine - Plant Hormone - Cytokine - BAP will increase plant growth, bud set, and in high dosage, stop the stretch period and cause your plants to stop growing vertically and start producing bud set almost immediately.

Ba 6 Benzylaminopurine-Plant Hormone-Cytokinin BAP Specification:

Product Name : Ba 6 Benzylaminopurine - Plant Hormone - Cytokinin- BAP
Storage Temperature: RT
CAS No: [1214-39-7]
Structure Formula: C12H11N5
Molecular Weight: 225.3
Soluble in 1N KOH @ 10 mg/mL
Appearance: White Fine Powder
Purity: 98%
Melting point: 230-233°C

Usage of Ba 6 Benzylaminopurine - BAP:

Benzylaminopurine is NOT water soluble. Use KOH Solution to dissolve.
Can be used in the vegetative growth or flower stages.
Can be used in drench feeds, hydroponic systems, soil, coco, soil-less mediums, and foliar sprays.


Foliar Spray:Once every 7-14 days


Furfurylaminopurine (Kinetin) 99% – Cytokinin Kinerase

Physical state and appearance: Solid.
Odor: Not available.
Taste: Not available.
Molecular Weight: 215.22 g/mole
Color: White.
pH (1% soln/water): Not available.
Boiling Point: Not available.
Melting Point: 270°C (518°F)
Critical Temperature: Not available.
Specific Gravity: Not available.
Vapor Pressure: Not applicable.
Vapor Density: Not available.
Volatility: Not available.
Odor Threshold: Not available.
Water/Oil Dist. Coeff.: Not available.
Ionicity (in Water): Not available.
Dispersion Properties: See solubility in water.
Solubility: Partially soluble in cold water.
Section

Kinetin is a synthetic cytokinin class plant growth regulating phytohormone, altough it has been shown to exist naturally in the DNA of cells of almost all organisms tested so far, including human and numerous plants.

Kinetin is currently sold commercially under the trade name "Bonide Tomato and Blossom Set Spray", and can be used to increase yields of various fruits and vegetables, produce seedless fruits, and increase 'budding' of various herbs.
Kinetin is also widely used in producing new plants from tissue cultures.

Disclaimer:
This is Dependant on timing - Strain - Other Hormones used
 
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shaggyballs

Active member
Veteran
Gibberellins


Speculative Overall Role

Sugar deficiency signal in the same pathway of action as brassinosteroid.

Growth Direction Tendencies are Lengthening or elongating.
What is gibberellin's complementary stimulating hormone?

Jasmonic Acid/Jasmonate

If overall speculative role is true, where, when and which cells should synthesize gibberellins Acid?

Darkened plants should have high levels of GA, well lighted plants, low levels. Like abundance signals GA may be mostly made in meristematic cells and much less so as cells mature. (Or for real theoretical beauty, deficiency hormones should be made mostly in mature cells and much less so in meristematic cells). GA should be made when a cell has less than enough sugar to support both it any cell dependent on it for sugar acquisition. Thus GA is an indication that sugar exists in less than enough amounts to continue the plant at its current size, thus the plant must use emergency stores of starch, find new sources of the molecule and cut down on its sinks.

If overall speculative role is true, what should gibberellins exogenous treatment produce?

High levels of exogenously applied GA should induce JA synthesis,because many of GA's effects may be to increase sugar levels within the plant, if only temporarily. This may include making dormant reactions that normally depend on sugar.

If overall speculative role is true, what should gibberellins inhibit and stimulate?

GA should encourage shoot and new shoot growth, but inhibit root growth and even encourage root senescence. This may be a particularly apparent when ethylene levels are high and strigolactone and ABA levels are low and levels low as this is an indication that resources need to rerouted from the root to the shoot.

If overall speculative role is true, how should gibberellins affect storage?

GA should cause the emptying of stored sugar reserves found in vacuoles or tubers.

If overall speculative role is true, how should gibberellins be transported?

Sugar deficiency, on average should be detected in the roots first, the point furthest from the source of sugar. GA may be transported from the roots to the shoots where presumably they repel sugar and send it in the opposite direction back to the low sugar roots.

If overall speculative role is true, how should gibberellins affect nutrient attraction and repulsion?

GA should generally push all nutrients and abundance signals/hormones out of cells. GA should attract the deficiency signals/hormones, ABA, ET and strigolactones, leading to positive feedback and cell senescence. GA should perhaps also work with JA to attract nutrients and positive hormones to leaves that are making jasmonic acid and thus are efficient synthesizers of sugar.

If overall speculative role is true, how should gibberellins affect apical dominance?

GA should break shoot apical dominance because low sugar levels are an indication of poor performance by the currently dominant apical shoot. GA may strengthen the currently dominant root apices in order not to encourage any new root growth which would be a further sink on sugar levels.

If overall speculative role is true, how should gibberellins affect Cell Division?

Although it may encourage cell division in the shoots, if it is inducing new ones, GA should generally inhibit cell division, as a sugar deficient plant is in no condition to expand.

If overall speculative role is true, how should gibberellins affect Senescence

Just as I am hypothesizing that SA, JA, IAA and CK all need to be present to induce cell division, ABA, GA/BR, ET and strigolactone may all need to be present for cell senescence to proceed. GA/BR should encourage senescence, particularly of root tissue whose nutrients can be cannibalized and used to make more sugar producing shoot and leaf tissue.

If overall speculative role is true, how should GA effect growth
directions to provide balance in the plant?

Gibberellin is well know to lengthen leaves and stems. Presumably stem lengthening accomplishes moving shaded plants back into the sunlight.

Proven Synthesis and Transport

GA levels go up in the dark when Sugar cannot be manufactured and down in the light. 20 Why this makes sense - GA is another deficiency hormone that is presumably active at night when sugar can't be made and so continual maintenance metabolism must be carried out by dissolving sugar store stored during the day. GA induces this storage use.

"The highest content of GA was characteristic of leaves in the period of growth cessation." 31 Why this makes sense - Growth cessation I is a prelude to senescence. Presumably normally leaf senescence is initiated by ABA and strigolactones but as indicated elsewhere these hormones probably push out all nutrients and attract deficiency hormones. There may be two phases of senescence, growth senescence/hibernation and secondly actual senescence. Growth cessation or hibernation may be a valley with steep hills to overcome either to get back to growing, or to initiate final senescence.

Proven Effects

Promotes shoot and flower stem lengthening especially in the dark. Why this makes sense - This moves the plant stem and leaves back into the sun out of the shade.

Greatly promotes bud growth.
Why this makes sense - The hydrolyzing of starch may be a prelude to bud growth in the spring. Additionally the need for new buds before the winter begins may be signaled by increasing levels of GA which indicates the plant is using more and more stored sugar and less newly photosynthesized glucose which in turn is an indication of the coming winter.

GA reverses ABA effects on growth inhibition and dormancy. Why this makes sense - GA hydrolyzes stored starch. This freed sugar may stimulate breaking of dormancy.

Dissolves stored starch.
Why this makes sense - Dissolved stored starch makes up for sugar gap.

At low concentrations GA (gibberellin A3) and other gibberellins promote lateral root growth but high concentrations markedly inhibit it.
Why this makes sense - At low levels, hydrolyzed stored starch frees the root from lateral root growth limiting sugar levels. At high levels the plant know it is experiencing severe sugar shortages so need to concentrate resources toward the sugar producing shoot.
 

shaggyballs

Active member
Veteran
Gibberellins

During the 1930s Japanese scientists isolated a growth-promoting substance from cultures of a fungus that parasitizes rice plants. They called it gibberellin.

After the delay caused by World War II, plant physiologists in other countries succeeded in isolating more than 30 closely-related compounds. One of the most active of these — and one found as a natural hormone in the plants themselves — is gibberellic acid (GA).

GA has a number of effects on plant growth, but the most dramatic is its effect on stem growth. When applied in low concentrations to a bush or "dwarf" bean, the stem begins to grow rapidly. The length of the internodes becomes so great that the plant becomes indistinguishable from climbing or "pole" beans. GA seems to overcome the genetic limitations in many dwarf varieties.

Synthesis of gibberellins also helps grapevines climb up toward the light by causing meristems that would have developed into flowers to develop into tendrils instead.

One of the 7 pairs of traits that Mendel studied in peas as he worked out the basic rules of inheritance was dwarf-tall. The recessive gene - today called le - turns out to encode an enzyme that is defective in enabling the plant to synthesize GA. The dominant gene, Le, encodes a functioning enzyme permitting normal GA synthesis and making the "tall" phenotype.
Effects of gibberellins on gene expression

Gibberellins exert their effects by altering gene transcription.

The steps:
Gibberellin enters the cell and
binds to a soluble receptor protein called GID1 ("gibberellin-insensitive dwarf mutant 1") which now can bind to a
complex of proteins (SCF) responsible for attaching ubiquitin to one or another of several DELLA proteins.
This triggers the destruction of the DELLA proteins by proteasomes.
DELLA proteins normally bind gibberellin-dependent transcription factors, a prominent one is designated PIF3/4, preventing them from binding to the
DNA of control sequences of genes that are turned on by gibberellin.
Destruction of the DELLA proteins relieves this inhibition and
gene transcription begins.
This mechanism is another of the many cases in biology where a pathway is turned on by inhibiting the inhibitor of that pathway (a double-negative is a positive).

Another example: Auxin.
Although most of the specific proteins involved are quite different, both gibberellins and auxin affect gene expression by a similar mechanism of relief of repression.



The Nature of Gibberellins

Unlike the classification of auxins which are cassified on the basis of function, gibberellins are classified on the basis of structure as well as function. All gibberellins are derived from the ent-gibberellane skeleton. The structure of this skeleton derivative along with the structure of a few of the active gibberellins are shown above. The gibberellins are named GA1....GAn in order of discovery. Gibberellic acid, which was the first gibberellin to be structurally characterised , is GA3. There are currently 136 GAs identified from plants, fungi and bacteria.

Gibberellin Biosynthesis and Metabolism

Gibberellins are diterpenes synthesized from acetyl CoA via the mevalonic acid pathway. They all have either 19 or 20 carbon units grouped into either four or five ring systems. The fifth ring is a lactone ring as shown in the structures above attached to ring A. Gibberellins are believed to be synthesized in young tissues of the shoot and also the developing seed. It is uncertain whether young root tissues also produce gibberellins. There is also some evidence that leaves may be the source of some biosynthesis (Sponsel, 1995; Salisbury and Ross). The pathway by which gibberellins are formed is outlined below and illustrated in figure1.
3 acetyl CoA molecules are oxidized by 2 NADPH molecules to produce 3 CoA molecules as a side product and mevalonic acid.
Mevalonic acid is then Phosphorylated by ATP and decarboxylated to form isopentyl pyrophosphate.
4 of these molecules form geranylgeranyl pyrophosphate which serves as the donor for all GA carbon atoms.
This compound is then converted to copalylpyrophosphate which has 2 ring systems
Copalylpyrophosphate is then converted to kaurene which has 4 ring systems
Subsequent oxidations reveal kaurenol (alcohol form), kaurenal (aldehyde form), and kaurenoic acid respectively.
Kaurenoic acid is converted to the aldehyde form of GA12 by decarboxylation. GA12 is the 1st true gibberellane ring system with 20 carbons.
From the aldehyde form of GA12 arise both 20 and 19 carbon gibberellins but there are many mechanisms by which these other compounds arise.
Certain commercial chemicals which are used to stunt growth do so in part because they block the synthesis of gibberellins. Some of these chemicals are Phosphon D, Amo-1618, Cycocel (CCC), ancymidol, and paclobutrazol. During active growth, the plant will metabolize most gibberellins by hydroxylation to inactive conjugates quickly with the exception of GA3. GA3 is degraded much slower which helps to explain why the symptoms initially associated with the hormone in the disease bakanae are present. Inactive conjugates might be stored or translocated via the phloem and xylem before their release (activation) at the proper time and in the proper tissue (Arteca, 1996; Sponsel, 1995).

Functions of Gibberellins

Active gibberellins show many physiological effects, each depending on the type of gibberellin present as well as the species of plant. Some of the physiological processes stimulated by gibberellins are outlined below (Davies, 1995; Mauseth, 1991; Raven, 1992; Salisbury and Ross, 1992).

Stimulate stem elongation by stimulating cell division and elongation.
Stimulates bolting/flowering in response to long days.
Breaks seed dormancy in some plants which require stratification or light to induce germination.
Stimulates enzyme production (a-amylase) in germinating cereal grains for mobilization of seed reserves.
Induces maleness in dioecious flowers (sex expression).
Can cause parthenocarpic (seedless) fruit development.
Can delay senescence in leaves and citrus fruits.
 

shaggyballs

Active member
Veteran
Ethylene

Ethylene is a plant hormone that differs from other plant hormones in being a gas.

It has the molecular structure:

H2C=CH2

As they approach maturity, many fruits (e.g., apples, oranges, avocados) release ethylene.

Ethylene then promotes the ripening of the fruit.

Commercial fruit growers can buy equipment to generate ethylene so that their harvest ripens quickly and uniformly.
The presence of ethylene is detected by transmembrane receptors in the endoplasmic reticulum (ER) of the cells. Binding of ethylene to these receptors unleashes a signaling cascade that leads to activation of transcription factors and the turning on of gene transcription.

The ill-fated FlavrSavr tomato contains an antisense transgene that interferes with the synthesis of ethylene and hence slows ripening.

Ethylene also affects many other plant functions such as:
abscission of leaves, fruits, and flower petals;
drooping of leaves;
sprouting of potato buds;
seed germination;
stem elongation in rice (by promoting the breakdown of abscisic acid (ABA) and thus relieving ABA's inhibition of gibberellic acid);
flower formation in some species.

Speculative Overall Role

Oxygen deficiency signal as well as possbily excess carbon dioxide signal in the root.

Growth Direction Tenancies are Broadening or widening.
What is ethylene's speculative complementary abundance signal?

Auxin (IAA)

If overall speculative role is true, where,when and which cells should synthesize ethylene?

Cells most apt to be oxygen deficient are the interior of roots and flooded roots in general.

If overall speculative role is true, what
should exogenous ethylene treatment produce?

Exogenous ethylene treatment should show methods for increasing oxygen to the roots such as aerenchyma tubes or increasing leaf area. Additional measures might include epinasty for pumping out extra water from around the roots, metabolism inhibition and photosynthesis stimulation.

If overall speculative role is true, what should ethylene inhibit and stimulate?

Ethylene should inhibit root growth and encourage shoot growth. It should inhibit metabolism and stimulate photosynthesis. It also is known to stimulate the growth of root hairs, a method for increasing the surface area of the root and its absorption of oxygen for local use.

If overall speculative role is true, how should ethylene affect storage?

Ethylene should cause the release of stored oxygen if there is such a thing.

If overall speculative role is true, how should ethylene be transported?

Ethylene should be transported from the roots to the shoots, perhaps by rising or bubbling up from the ground as a gas or being transported up as ACC.

If overall speculative role is true, how should ethylene affect attraction and repulsion?

Ethylene should generally push nutrients and stimulating/growth hormones out of cells and attract deficiency hormones. Possibly it works with auxin producing leaves to attract more nutrients to these oxygen harvesting sites.

If overall speculative role is true, how should ethylene affect apical dominance?

Ethylene represents a failure of the current methods for harvesting oxygen, therefore it should break the apical dominance induced by auxin.

If overall speculative role is true, how should ethylene affect Cell Division?

Ethylene should generally inhibit cell division although it may stimulate it in shoot areas that are particularly efficient at harvesting oxygen and therefore making auxin.

If overall speculative role is true, how should ethylene affect senescence?

Ethylene should inhibit root growth along with gibberellin and cause the senescence of older roots. It should inhibit the senescence of shoots parts, especially those making auxin.

If overall speculative role is true, how should ethylene effect growth directions to provide balance in the plant?

Ethylene is known to broaden plant parts. Its analogue stimulating hormone, auxin, appropriately lengthens plant cells and tissues.

Proven Synthesis and Transport

Induced by high levels of auxin, especially in the roots but this can be moderated by red light which is characteristic of shading.
Why this makes sense - auxin is an indicator of oxygen abundance so, oxygen requiring reactions are stimulated, depleting oxygen levels. Why shading would moderate might be because oxygen reactions are less stimulated under cooler temperatures so if the plant senses shade it prepares itself for less oxygen use.

Ethylene levels increase during flooding, probably due to entrapment rather anoxia. Most plant appear to have a net inhibition of ethylene production under anoxic or carbon dioxide deficient conditions.
Why this makes sense - This doesn't make sense and my theory suggest that the finding is wrong.

Proven Effects

Promotes the ripening of fruit with climacteric respiration releasing additional ethylene.
Why this makes sense - Any of the deficiency hormone should be able to lead to a ripening process which might essentially be a kind of programmed cell death and a freeing up of internal stores of nutrients within cells. However the advantage of ethylene is that it is a gas and can effect neighboring fruit. Additionally if there are interstitial gas spaces, the hormone would be rapidly transported throughout the fruit. The increase in respiration supposedly induced by Ethylene in fruits, might be relatively unique to fruits as most other plant parts according to my theory should have their respiration inhibited.

Broadens/thickens plant parts.
Why this makes sense - Each of the abundance, deficiency pairs have opposite patterns of growth. If Auxin effects on the growth of the plant aren't producing the results needed then ETH takes over to try to do better growing the plant leaves and roots wider instead of auxin's longer. Also ETH and GA are the two root deficiency signals and they also show a balanced opposite pattern of growth with GA lengthening plant parts as well.

Inhibits leaf expansion.
Why this makes sense - This doesn't make too much sense in that my assumption is an expanded leaf should take in more oxygen which it can transport to the root.

Inhibits Geo-tropism. Inhibits auxin transport and production? Why this makes sense - Geo-tropism is the growth of the root downward which is opposite the direction of the greatest amounts of oxygen, so this makes sense to be inhibited. The inhibition of transport and synthesis and Auxin makes sense as a negative feedback on Auxin which is stimulating too much oxygen use if Oxygen levels fall and Ethylene is synthesized.

Induces leaf, fruits, and flower petal abscission.
Why this makes sense - as mentioned any of the deficiency hormones should be capable of being the leader in cell or plant part death. However, Ethylene as a respiration damper might always be the last step in apotheosis.

Stimulates seed germination.
Why this makes sense - This doesn't make too much sense if Ethylene is a respiration damper, however, maybe at low levels it increases the access of the seed to oxygen through various mechanisms, including possibly stored oxygen if there is such a thing.

Flooding produces the epinasty reaction through ethylene, where leaf surfaces deliberately grow from a position perpendicular to the stem to one which is more horizontal.
Why this makes sense - Epinasty may increase the wind resistance of the leaves by putting them in the path of the wind intend of parallel to it. Perhaps this increases oxygen absorption. Additionally the action of the wind on the leaves in its path, may act like a long handled water pump. The leaves would be the water pump handle. May be there is a one way valve in the leaf stem which caused the wind stretched water column in the leaf remain in the leaf once the water column is compressed when the leaf snaps back to a horizontal plane from the action of a gust of wind. The total effect might be to pump more water out of water logged roots.

Induces air spaces called aerenchyma used for gas diffusion in roots during flooding of non-water based plants.
Why this makes sense - increases oxygen flow from the leaves, shoots and adventitious roots.

Carbon dioxide inhibits ethylene action.
Why this makes sense - This doesn't make sense if Ethylene is an indicator of anoxia as carbon dioxide should be a confirmation of anoxic conditions. However if ethylene is an indicator of all gas deficiency, perhaps as more an indicator of carbon dioxide deficiency in the shoot and oxygen in the root, it might make sense.

Inhibits embryogenesis of cell cultures.
Why this makes sense - embryogenesis is perhaps a respiration intensive process.

Induces root hair growth.
Why this makes sense - Oxygen can be more adequately absorbed from spaces between soil particles if root hairs grow out.

Ethylene up-regulates auxin bio-synthesis at least in the roots. 61 Why this makes sense - This doesn't make sense unless the total effect of ethylene is to change plant behavior to procure more oxygen and eventual success at this should re-stimulate if indirectly, the synthesis of auxin.

Flood induced ethylene sensitizes plants to the existing steady auxin levels, inducing adventitious roots formation. Why this makes sense - Adventitious roots are roots which exit the stem of the plant above the flood line and go back into the water. Presumably these roots have better access to oxygen enabling them to use respiration to absorb water and minerals better. Also the adventitious roots may directly absorb oxygen above the flood level and bring it to the aerenchyma to the help oxygen starved conventional roots.

Induces flower formation in some species.
Why this makes sense - Many plants will flower under duress. This is conceivably because the plant "calculates" that conditions might get worse and eventually make life inviable thus it better get reproduction over with so that it can produce tough seed which can withstand the adverse seasons in the environment and start over when conditions improve again.

Etephon (ethylene precursor) has a dual role in tuberization. It promotes already formed tubers by inhibiting stolon growth. Differently though it inhibits the formation of new tubers. 64 Why this makes sense - Tubers may be a strategy for a plant to last through the parts of the year like the winter when conditions or adverse for the species. The ethylene being an indicator of difficulty procuring adequate oxygen from the environment, should promote th plant going into dormancy through building up of its tuber. New tubers or stolons are probably more vulnerable to adverse conditions having a great surface area per weight ratio. Thus the plant wisely concentrates on those tubers it already has rather than trying to branch out and create new ones.



Nature of Ethylene

Ethylene, unlike the rest of the plant hormone compounds is a gaseous hormone. Like abscisic acid, it is the only member of its class. Of all the known plant growth substance, ethylene has the simplest structure. It is produced in all higher plants and is usually associated with fruit ripening and the tripple response

History of Discovery in Plants

Ethylene has been used in practice since the ancient Egyptians, who would gas figs in order to stimulate ripening. The ancient Chinese would burn incense in closed rooms to enhance the ripening of pears. It was in 1864, that leaks of gas from street lights showed stunting of growth, twisting of plants, and abnormal thickening of stems (the triple response)(Arteca, 1996; Salisbury and Ross, 1992). In 1901, a russian scientist named Dimitry Neljubow showed that the active component was ethylene (Neljubow, 1901). Doubt discovered that ethylene stimulated abscission in 1917 (Doubt, 1917). It wasn't until 1934 that Gane reported that plants synthesize ethylene (Gane, 1934). In 1935, Crocker proposed that ethylene was the plant hormone responsible for fruit ripening as well as inhibition of vegetative tissues (Crocker, 1935). Ethylene is now known to have many other functions as well.

Biosynthesis and Metabolism

Ethylene is produced in all higher plants and is produced from methionine in essentially all tissues. Production of ethylene varies with the type of tissue, the plant species, and also the stage of development. The mechanism by which ethylene is produced from methionine is a 3 step process (McKeon et al., 1995; Salisbury and Ross, 1992).
ATP is an essential component in the synthesis of ethylene from methionine. ATP and water are added to methionine resulting in loss of the three phosphates and S-adenosyl methionine.
1-amino-cyclopropane-1-carboxylic acid synthase (ACC-synthase) facilitates the production of ACC from SAM.
Oxygen is then needed in order ro oxidize ACC and produce ethylene. This reaction is catalyzed by an oxidative enzyme called ethylene forming enzyme.
The control of ethylene production has received considerable study. Study of ethylene has focused around the synthesis promoting effects of auxin, wounding, and drought as well as aspects of fruit-ripening. ACC synthase is the rate limiting step for ethylene production and it is this enzyme that is manipulated in biotechnology to delay fruit ripening in the "flavor saver" tomatoes (Klee and Lanahan, 1995).

Functions of Ethylene

Ethylene is known to affect the following plant processes (Davies, 1995; Mauseth, 1991; Raven, 1992; Salisbury and Ross, 1992):

Stimulates the release of dormancy.
Stimulates shoot and root growth and differentiation (triple response)
May have a role in adventitious root formation.
Stimulates leaf and fruit abscission.
Stimulates Bromiliad flower induction.
Induction of femaleness in dioecious flowers.
Stimulates flower opening.
Stimulates flower and leaf senescence.
Stimulates fruit ripening.


spurr says:
AFAIU it doesn't affect cananbis plants it in a 'good' manner when we are growing for buds, very little ethylene should be the goal for growing cannabis. But for sex reversal, etc., it can be have an affect. Here is something I wrote about ethylene in the Co2 thread:

---------------------------------
"It [ethylene] is produced by the plant and affects maturation, senescence and abscission of leafs and flowers. Ethylene buildup also hinders auxin transport if ethylene is built up too high. Ethylene buildup can also reduce flower size. It's a good idea to vent the room at least once a day, esp. in latter stages of flowering to remove buildup of ethylene.


Here are a couple of ethylene refs.:

1. "Ethylene In The Greenhouse": The authors explain how to detect ethylene, how to take action against it and how to stop problems before they happen.
By W. Roland Leatherwood and Neil S. Mattson
April 2010
https://www.greenhousegrower.com/magazine/?storyid=3153

2. "Ethylene, Plant Senescence and Abscission"
Stanley P. Burg
Plant Physiol. 1968 September; 43(9 Pt B): 1503–1511.
https://www.ncbi.nlm.nih.gov/pmc/arti...00512-0034.pdf"
 

shaggyballs

Active member
Veteran
Types of ethylene

Ethephon

2-chloroethyl phosphonic acid

Chemical Class/Use: organic phosphorus compound/plant growth regulator

EPA report

The EPA has determined that there is limited potential for risk to certain nontarget plants from use of ethephon on cotton, macadamia nuts, pineapples, tobacco,blackberries and apples in North Carolina.

The registrant has proposed reducing the use rate on blackberries
and on apples in North Carolina.

In addition the Agency has reviewed information provided by the registrant indicating that maximum use rates of ethephon are only required when certain weather conditions exist.
The Agency has determined that most uses of ethephon would be below the maximum rate and the risk quotient would, therefore, be below the Agency's level of concern.

The Agency has concluded that with these risk reduction measures the risk to nontarget plants from the use of ethephon will be limited.

Ethephon was classified as a Group D chemical (indicating insufficient weight of evidence of carcinogenicity for humans) based on available data. A Reference Dose (RfD) was established as 0.018 mg/kg/day based on clinical signs of toxicity observed at 1.8 mg/kg/day in a 28-day oral human study.

An uncertainty factor of 100 was used to account for intraspecies variability and the lack of a NOEL.
The Agency has conducted acute dietary exposure and risk assessments using USDA food consumption information to estimate the distribution of single day exposures through the diet for the U.S. population and certain subgroups.

The one day dietary endpoint of concern of 1.8 mg/kg/day, based on cholinergic effects was derived from a 28-day oral human toxicity study.

Margins of exposure (MOE), estimates of how closely exposure comes to the dose of concern (1.8 mg/kg/day), were calculated for various population subgroups.

Agency estimates indicate that acute dietary exposures to infants (less than 1 year of age) may be of concern when the 95th percentile of exposure is used. However, the Agency has employed numerous conservative assumptions in calculating the acute dietary risk relative to the exposure.

The Agency assumed that all food crops on which ethephon is registered have been treated with ethephon and that maximum residue levels reported in or on unwashed, unpeeled, uncooked commodities at the farm gate are present on all foods. However usage data indicate that the treatment percentage of major infant foods on which ethephon is registered is < 10% or even"negligible".
The probable residue dilution that occurs in processed infant foods was not taken into account.

In addition, ethephon degrades fairly rapidly to ethylene,phosphate and chloride in neutral and alkaline environments.
Therefore, by the time the food has cleared distribution channels and/or processing plants, residues at the dinner table are likely to be significantly lower than high-end levels at the farm gate.

The Agency believes that the acute dietary risk values for infants listed in Section III, B, 3 of this document represent an
unrealistic worst case situation and actual risks to infants are likely to be minimal.

A 48 hour restricted-entry interval (REI), as imposed by the Worker Protection Standard (WPS), will be retained based on potential eye and skin irritation concerns.
The Agency has determined that this 48-hour REI must be increased to 72 hours when ethephon is applied outdoors in arid areas.
In addition, since ethephon is classified as toxicity category I for eye irritation potential, protective eyewear is now required
.
Because there are no toxicological endpoints of concern for dermal (systemic) or inhalation toxicity, the Agency has determined that mixer/loader/applicator and post application/reentry data are not required to support the reregistration of ethephon.

List of Brand Name Products which Contain this Chemical

PREP BRAND ETHEPHON FOR COTTON AND TOBACCO
http://iaspub.epa.gov/apex/pesticides/f?p=PPLS:102:::NO::P102_REG_NUM:264-418
https://www.google.com/url?sa=t&rct...6EE7UuLhmdMU234ghUAKSZQ&bvm=bv.57155469,d.eW0



What is Ethrel?

Ethrel (also Ethephon) is a trade name for 2-chloroethylphosphonic acid, a compound that slowly releases ethylene gas. Ethylene gas is a naturally occuring plant hormone that is associated with fruit ripening, among many other normal plant functions.

Directions for Use

Sow seeds in usual sterile seeding mix. Water using a 1 mM solution of ethrel (1 mM = 1 millimolar = 1 gram powder in 6 litres of water). Enclose seedflat in plastic bag and place in a refrigerator for 2 weeks. Arrange for the refrigerator light to stay on 24 hours a day. Water with the ethrel solution if the sowing medium shows signs of drying. After 2 weeks, expose seedflat to room temperature and normal light. Germination should be complete in 2-4 weeks.

Where to Get Ethrel?

CANADA: Plant Products (905-793-7000) sells Ethrel under the trade name “Ethephon”.

CANADA and U.S.A.: Sigma Scientific of St. Louis (1-800-325-3010) will sell small quantities to any address in Canada and the United States. The catalogue number is C0143 and the listing is under 2-chloroethylphosphonic acid. The smallest quantity available is 100 mg.

Is Ethrel Considered Organic?

Not likely, but check with your organic certifying agency for a ruling.

I believe this to be the best choice,due to the hope it has been tested under combustion conditions.

More info about Ethephon!

We studied the effect of ethephon on levels of the major cannabinoids (tetrahydrocannabinol and cannabidiol) and chlorophyll, carotenoids and α-tocopherol in Cannabis sativa at productive stage. Results revealed that ethephon increased THC content of leaf in male and female plants and of male flowers. However, ethephon unable to enhancing THC content in female flowers. Treatment with etheohon increased CBD content in male and female leaf and female flowers. The treatment of male flowers with low ethephon concentration caused an increase, and those treated with high ethephon concentration resulted in a decrease in CBD content. The lowest level of ethephon (1μM) enhanced chlorophyll a, b and total chlorophyll in male and female plants. Both sexes treated with ethephon showed an increase in carotenoids content, but 1μM ethephon had the stronger effect in this regards. Male and female plants had a higher content of α-tocopherol when treated with ethephon. These results showed ethephon is a suitable treatment for increasing cannabinoids and α-tocopherol in productive stage of cannabis and there was not a relation between primary and secondary terpenoids.

https://www.google.com/url?sa=t&rct...9IvfskyH_YqSsWtwXLb-pmw&bvm=bv.57155469,d.eW0
https://www.icmag.com/ic/showthread.php?t=119290
 
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shaggyballs

Active member
Veteran
Abscisic Acid

Speculative Overall Role

Water deficiency signal
Growth Direction Tendencies Broadening or widening
What is ABA's speculative
complementary abundance signal?

Salicylic Acid (SA)

If overall speculative role is true, where,
when and which cells should synthesize ABA?

Dry plants should have high levels of ABA, well watered plants, low levels. Like abundance signals ABA may be mostly made in meristematic cells and much less so as cells mature. (Or for real theoretical beauty, deficiency hormones should be made mostly in mature cells and much less so in meristematic cells). ABA should be made when a cell has less than enough water to support both it any cell dependent on it for water acquisition. Thus ABA is an indication that water exists in less than enough amounts to continue the plant at its current size, thus the plant must use emergency stores of water, find new sources of the liquid and cut down on water sinks.

If overall speculative role is true, what
should exogenous ABA treatment produce?

High levels of exogenously applied ABA should induce ABA synthesis, because many of ABA's effects may be to increase water levels within the plant, if only temporarily. This may include making dormant reactions that are normally dependent on water.

If overall speculative role is true, what
should ABA inhibit and stimulate?

ABA should encourage root and new root growth, but inhibit shoot growth and even encourage shoot and leaf senescence.

If overall speculative role is true,
how should ABA affect storage?

ABA should cause the emptying of stored water reserves found in vacuoles or tubers.

If overall speculative role is true,
how should ABA be transported?

Good question. Perhaps, operationally water is more a problem for the shoots than the roots so greater amounts of ABA exist there and the target of operation is mainly the roots so it get transported down.

If overall speculative role is true, how should
ABA affect attraction and repulsion?

ABA should generally push all nutrients and abundance signals/hormones out of cells. The pushing out of minerals, sugar and oxygen should lead to an explosion of scarcity hormones and a rapid emptying of cell nutrients. Speculatively maybe ABA has no effect on immature tissues or actually stimulates the uptake of water and maybe less so, other nutrients and hormones to these vulnerable cells. Working perhaps especially with root cells that produce salicylic acid to attract nutrient and growth hormones to efficient water harvesting roots.

If overall speculative role is true, how
should ABA affect apical dominance?

Should break root apical dominance because low water levels are an indication of poor performance by the currently dominant apical root. ABA may strengthen the currently dominant shoot apex in order not to encourage any new shoot growth which would be a further sink on water levels.

If overall speculative role is true, how
should ABA affect Cell Division?

Although it may encourage it in the roots, if it is inducing new ones, ABA should generally inhibit cell division, as a water deficient plant is in no condition to expand.

If overall speculative role is true, how
should ABA affect senescence?

Just as I am hypothesizing that ABA, JA, IAA and CK all need to be present to induce cell division, ABA, GA/BR, ET and strigolactones may all need to be present for cell senescence to proceed. ABA should encourage senescence, particularly of shoot tissue whose nutrients can be cannibalized and used to make more water absorbing root tissue. Since water is the issue a relative net preserving of roots should occur.

If overall speculative role is
true, how should ABA effect growth
directions to provide balance in the plant?

Since GA/BR causes lengthening, ET broadening, strigolactones lengthening, what's left is ABA should cause cell and tissue broadening when it induces growth if it does. (I believe I may have seen such a finding but I have to find the reference again).

Proven Synthesis and Transport

Under consistent levels of desiccation, ABA levels normally peak at night. 1 Why this might make sense - ABA like the other insufficiency hormones, are more active at night where nutrient stores have to be relied on to support life, rather than during the days when they are actively acquired.

Closes stomata via ABA synthesized in the root. 2 Why this might make sense - having closed stomates cuts off excess transpiration and net water loss (insufficient water replacement occurring in the roots).

Induce by drought. Why this makes sense - of course drought often induces water shortages in plants.

ABA coming up from the root, synergizes with auxin coming down from the apex to produce apical dominance. Why this makes sense - ABA probably along with another of the shortage hormones, maintains apical dominance in the shoot at night in order

Proven Effects

Closes stomata via ABA synthesized in the root. Why this might make sense - So water loss is slowed by closing of the stomata.

At high concentrations, inhibits root growth, but after removal, stimulates greater root lengthening and branching than controls. Why this might make sense - ?

Mediate adaptation to salt. Why this might make sense - High salt levels may water stress plants.

Mediate adaptation to heat. Why this might make sense - High salt levels may water stress plants.

Mediate adaptation to cold. Why this might make sense - Cold may make water less available to plants. Transpiration cools plants, so this might be avoided by the ABA induced stomata closing.

Inhibits kinetin nucleotide formation. 8 Why this might make sense - The photosynthesis process uses twice as much water as it makes and kinetin stimulates this.

Down regulates enzymes needed for photosynthesis. Why this might make sense - photosynthesis uses up water as the hydrogen atoms are donated to the sugar molecules with the added energy of the sun. The plant probably dials down growth supporting photosynthesis to levels just needed for survival, in order not to use up water it can't afford.

Induces bud dormancy. Lower levels of ABA is associated with dormancy termination in winterized plants. 10 Why this might make sense - ABA's effect overall maybe to lower metabolism to a hibernating level. This is in part because photosynthesis uses up water. Metabolism allows you to get it back, but photosynthetic levels high enough to allow growth would use up water which is in short supply during droughts, at night and presumably during the winter. Also even some metabolism will produce toxic wastes which will take more energy and water loss to remove. Therefore the tree may want to be in a state of hibernation during the winter which ABA helps maintain.

ABA Promotes tuberization. Why this might make sense - it encourages the plant to hibernate rather than use the net carbon gain from the formula photosynthesis - metabolism, for growth.

ABA coming up from the root, synergizes with auxin coming down from the apex to produce apical dominance. 12 Why this might make sense - the breaking of shoot apical dominance is probably only warranted under good root conditions, i.e. when there is more than enough water and minerals to support the cells in the root and shoot at their present weight.



Research in recent years on the biology of guard cells has shown that these specialized cells integrate both extra- and intra-cellular signals in the control of stomatal apertures. Among the phytohormones, abscisic acid (ABA) is one of the key players regulating stomatal function. In addition, auxin, cytokinin, ethylene, brassinosteroids, jasmonates, and salicylic acid also contribute to stomatal aperture regulation. The interaction of multiple hormones can serve to determine the size of stomatal apertures in a condition-specific manner.We need to further study the roles of different phytohormones and the effects of their interactions on guard cell physiology and function





Abscisic acid (ABA)


Unlike animals, plants cannot flee from potentially harmful conditions like

drought
freezing
exposure to salt water or salinated soil.
They must adapt or die.

The plant hormone abscisic acid (ABA) is the major player in mediating the adaptation of the plant to stress.

Here are a few examples.

1. Closing of stomata

Some 90% of the water taken up by a plant is lost in transpiration. Most of this leaves the plant through the pores — called stomata — in the leaf. Each stoma is flanked by a pair of guard cells. When the guard cells are turgid, the stoma is open. When turgor is lost, the stoma closes.
Discussion of gas exchange in the leaf.
In angiosperms and gymnosperms (but not in ferns and lycopsids), ABA is the hormone that triggers closing of the stomata when soil water is insufficient to keep up with transpiration.

The mechanism:
ABA binds to receptors at the surface of the plasma membrane of the guard cells.
The receptors activate several interconnecting pathways which converge to produce
a rise in pH in the cytosol;
transfer of Ca2+ from the vacuole to the cytosol.
These changes
stimulate the loss of negatively-charged ions (anions), especially NO3− and Cl−, from the cell and also
the loss of K+ from the cell.
The loss of these solutes in the cytosol reduces the osmotic pressure of the cell and thus turgor.
The stomata close.
2. Protecting cells from dehydration

ABA signaling turns on the expression of genes encoding proteins that protect cells — in seeds as well as in vegetative tissues — from damage when they become dehydrated.

3. Root growth

ABA can stimulate root growth in plants that need to increase their ability to extract water from the soil.

4. Bud dormancy

ABA mediates the conversion of the apical meristem into a dormant bud. The newly developing leaves growing above the meristem become converted into stiff bud scales that wrap the meristem closely and will protect it from mechanical damage and drying out during the winter.

ABA in the bud also acts to enforce dormancy so if an unseasonably warm spell occurs before winter is over, the buds will not sprout prematurely. Only after a prolonged period of cold or the lengthening days of spring (photoperiodism) will bud dormancy be lifted.

5. Seed maturation and dormancy

Seeds are not only important agents of reproduction and dispersal, but they are also essential to the survival of annual and biennial plants. These angiosperms die after flowering and seed formation is complete. ABA is essential for seed maturation and also enforces a period of seed dormancy. As we saw for buds, it is important the seeds not germinate prematurely during unseasonably mild conditions prior to the onset of winter or a dry season. ABA in the seed enforces this dormancy. Not until the seed has been exposed to a prolonged cold spell and/or sufficient water to support germination is dormancy lifted.

6. Abscission

ABA also promotes abscission of leaves and fruits (in contrast to auxin, which inhibits abscission). It is, in fact, this action that gave rise to the name abscisic acid.

The dropping of leaves in the autumn is a vital response to the onset of winter when ground water is frozen — and thus cannot support transpiration — and snow load would threaten to break any branches still in leaf.

Most nondeciduous species in cold climates (e.g., pines) have "needles" for leaves. These are very narrow and have a heavy waterproof cuticle. The shape aids in shedding snow, and the cuticle cuts down on water loss.
7. Seedling growth

ABA inhibits stem elongation probably by its inhibitory effect on gibberellic acid.

8. Apical dominance

ABA — moving up from the roots to the stem — synergizes with auxin — moving down from the apical meristem to the stem — in suppressing the development of lateral buds. The result is inhibition of branching or apical dominance.



ABA (Abscisic acid)

Using ABA as foliar generally isn't wise because it can reduce stomatal conductance quite a bit (make stoma close down).
 

shaggyballs

Active member
Veteran
Nature of Abscisic Acid

Abscisic acid is a single compound unlike the auxins, gibberellins, and cytokinins. It was called "abscisin II" originally because it was thought to play a major role in abscission of fruits. At about the same time another group was calling it "dormin" because they thought it had a major role in bud dormancy. The name abscisic acid (ABA) was coined by a compromise between the two groups. Though ABA generally is thought to play mostly inhibitory roles, it has many promoting functions as well(Arteca, 1996; Mauseth, 1991; Raven, 1992; Salisbury and Ross, 1992).

History of Abscisic Acid

In 1963, abscisic acid was first identified and characterized by Frederick Addicott and his associates. They were studying compounds responsible for the abscission of fruits (cotton). Two compounds were isolated and called abscisin I and abscisin II. Abscisin II is presently called abscisic acid (ABA)(Addicot, 1963). Two other groups at about the same time discovered the same compound. One group headed by Philip Wareing was studying bud dormancy in woody plants. The other group led by Van Steveninck was studying abscission of flowers and fruits from lupine. Plant physiologists agreed to call the compound abscisic acid (Salisbury and Ross, 1992).

Biosynthesis and Metabolism
ABA is a naturally occurring compound in plants. It is a sesquiterpenoid (15-carbon) which is partially produced via the mevalonic pathway in chloroplasts and other plastids. Because it is sythesized partially in the chloroplasts, it makes sense that biosynthesis primarily occurs in the leaves. The production of ABA is accentuated by stresses such as water loss and freezing temperatures. It is believed that biosynthesis occurs indirectly through the production of carotenoids. Carotenoids are pigments produced by the chloroplast which have 40 carbons. Breakdown of these carotenoids occurs by the following mechanism:
Violaxanthin is a carotenoid which has forty carbons.
It is isomerized and then split via an isomerase reaction followed by an oxidation reaction.
One molecule of xanthonin is produced from one molecule of violaxanthonin and it is uncertain what happens to the remaining biproduct.
The one molecule of xanthonin produced is unstable and spontaneously changed to ABA aldehyde.
Further oxidation results in ABA.
Activation of the molecule can occur by two methods. In the first method, an ABA-glucose ester can form by attachment of glucose to ABA. In the second method, oxidation of ABA can occur to form phaseic acid and dihyhdrophaseic acid.
The transport of ABA can occur in both xylem and phloem tissues. It can also be translocated through paranchyma cells. The movement of abscisic acid in plants does not exhibit polarity like auxins. ABA is capable of moving both up and down the stem (Walton and Li, 1995; Salisbury and Ross).

Functions of Abscisic Acid
The following are some of the phyysiological responses known to be associated with abscisic acid (Davies, 1995; Mauseth, 1991; Raven, 1992; Salisbury and Ross, 1992).

Stimulates the closure of stomata (water stress brings about an increase in ABA synthesis).
Inhibits shoot growth but will not have as much affect on roots or may even promote growth of roots.
Induces seeds to synthesize storage proteins.
Inhibits the affect of gibberellins on stimulating de novo synthesis of a-amylase.
Has some effect on induction and maintanance of dormancy.
Induces gene transcription especially for proteinase inhibitors in response to wounding which may explain an apparent role in pathogen defense.
 

shaggyballs

Active member
Veteran
Brassinolide

When given extra shots of the plant steroid brassinolide, plants "pump up" like major league baseball players do on steroids. Tracing brassinolide's signal deep into the cell's nucleus, researchers at the Salk Institute for Biological Studies have unraveled how the growth-boosting hormone accomplishes its job at the molecular level.

The Salk researchers, led by Joanne Chory, a professor in the Plant Molecular and Cellular Biology Laboratory and a Howard Hughes Medical Institute investigator, published their findings in this week's journal Nature.

"The steroid hormone brassinolide is central to plants' growth. Without it, plants remain extreme dwarfs. If we are going to understand how plants grow, we need to understand the response pathway to this hormone," says Chory. "This study clarifies what's going on downstream in the nucleus when brassinolide signals a plant cell to grow."

Brassinolide, a member of a family of plant hormones known as brassinosteroids, is a key element of plants' response to light, enabling them to adjust growth to reach light or strengthen stems. Exploiting its potent growth-promoting properties could increase crop yields or enable growers to make plants more resistant to drought, pathogens, and cold weather.

Unfortunately, synthesizing brassinosteroids in the lab is complicated and expensive. But understanding how plant steroids work at the molecular level may one day lead to cheap and simple ways to bulk up crop harvests.

Likewise, since low brassinolide levels are associated with dwarfism, manipulating hormone levels during dormant seasons may allow growers to control the height of grasses, trees or other plants, thereby eliminating the need to constantly manicure gardens.

Based on earlier studies, the Salk researchers had developed a model that explained what happens inside a plant cell when brassinolide signals a plant cell to start growing.

But a model is just a model. Often evidence in favor of a particular model is indirect and could support multiple models. Describing the components of the signaling cascade that relays brassinolide's message into a cell's nucleus, postdoctoral researcher and lead author of the study Grégory Vert, now at the Centre national de la recherche scientifique (CNRS) in Montpellier, France, said, "All the players are old acquaintances and we knew from genetic studies that they were involved in this pathway. But when we revisited the old crew it became clear that we had to revise the original model."

When brassinosteroids bind a receptor on the cell's surface, an intracellular enzyme called BIN2 is inactivated by an unknown mechanism. Previously, investigators thought that inactivation of BIN2, which is a kinase, freed a second protein known as BES1 from entrapment in the cytoplasm, the watery compartment surrounding a cell's nucleus, and allowed it to migrate or "shuttle" into the nucleus where it tweaked the activity of genes regulating plant growth.

A closer inspection, however, revealed that BIN2 resides in multiple compartments of a cell, including the nucleus, and it is there – not in the cytoplasm – that BIN2 meets up with BES1 and prevents it from activating growth genes. "All of a sudden the 'BES1 shuttle model' no longer made sense," says Vert, adding that it took many carefully designed experiments to convince himself and others that it was time to retire the old model.

A new picture of how brassinosteroids stimulate plant growth now emerges based on those experiments: steroid hormones are still thought to inactivate BIN2 and reciprocally activate BES1, but instead of freeing BES1 to shuttle into the nucleus, it is now clear that the crucial activation step occurs in the nucleus where BES1 is already poised for action. Once released from BIN2 inhibition, BES1 associates with itself and other regulatory factors, and this modified form of BES1 binds to DNA, activating scores of target genes.

Referring to the work of Vert and other members of the brassinosteroid team, Chory says, "The old model may be out, but Greg's new studies, together with those of former postdocs, Yanhai Yin and Zhiyong Wang, have allowed us to unravel the nuclear events controlling brassinosteroid responses at the genomic level. This turns our attention to the last mystery: the gap in our understanding of the events between steroid binding at the cell surface and these nuclear mechanisms."

Brassinosteroid functions in a broad range of disease resistance

Brassinolide (BL), considered to be the most important brassinosteroid (BR) and playing pivotal roles in the hormonal regulation of plant growth and development, was found to induce disease resistance in plants. To study the potentialities of BL activity on stress responding systems, we analyzed its ability to induce disease resistance in tobacco and rice plants. Wild-type tobacco treated with BL exhibited enhanced resistance to the viral pathogen tobacco mosaic virus (TMV), the bacterial pathogen Pseudomonas syringae pv. tabaci (Pst), and the fungal pathogen Oidium sp. The measurement of salicylic acid (SA) in wild-type plants treated with BL and the pathogen infection assays using NahG transgenic plants indicate that BL-induced resistance does not require SA biosynthesis. BL treatment did not induce either acidic or basic pathogenesis-related (PR) gene expression, suggesting that BL-induced resistance is distinct from systemic acquired resistance (SAR) and wound-inducible disease resistance. Analysis using brassinazole 2001, a specific inhibitor for BR biosynthesis, and the measurement of BRs in TMV-infected tobacco leaves indicate that steroid hormone-mediated disease resistance (BDR) plays part in defense response in tobacco. Simultaneous activation of SAR and BDR by SAR inducers and BL, respectively, exhibited additive protective effects against TMV and Pst, indicating that there is no cross-talk between SAR- and BDR-signaling pathway downstream of BL. In addition to the enhanced resistance to a broad range of diseases in tobacco, BL induced resistance in rice to rice blast and bacterial blight diseases caused by Magnaporthe grisea and Xanthomonas oryzae pv. oryzae, respectively. Our data suggest that BDR functions in the innate immunity system of higher plants including dicotyledonous and monocotyledonous species.

The interesting part is that Brass. doesn't use the salycilyic acid pathways, but does induce SAR.

Brassinosteroid:

This is a plant steroid, it boosts yield, growth, rate of photosynthesis, phototropism, stress resistance (abiotic and biotic), root induction and growth, etc.

Brassinosteroids (BRs) are probably my favorite PGR, along with tricontanol. Both can cause plants to strech if over applied...

There is a natural brassinosteroid called "brassinolide" (BL), it's probably the 'strongest' form of BR verses BR analogs like 24‐epibrassinolide (EBR). The main reason BR analogs are a good choice is they last a long time (length of bioavailability) in water. Whereas brassinoloide only lasts ~3-10 days in water until it's unavailable (it breaks down). That isn't much of an issue for us, because we apply it as a foliar spray, however, I plan to analytically test BL and EBR to see if there is a worthwhile difference in affects on plants this year.

From my non-analytical trails thus far, I see no difference between the various types of BRs.

Here are some possible benefits for plants (e.g., cannabis) from application of BR:

Increased yield
Increased disease resistance
Increased root growth for cuttings and growing plants
Increased light tracking by leafs (i.e., phototropism)
Increased rate of photosynthesis (Pn) by virtue of increased photon (light) usage, e.g., light-regulated gene expression
Increased stress resistance such as cold, drought, media salinity and biotic attack
Increased growth rate by action of BR as a growth regulator vis-a-vis control of light-regulated gene expression and cell elongation
 

shaggyballs

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24-Epibrassinolide - Brassinolide - BRASS - BL

Speculative Overall Role

Sugar deficiency signal in the
same pathway of action as gibberellin

Growth Direction Tendencies Lengthening or elongating
What is brassinosteroid speculative
complementary abundance signal?

Jasmonic acid/Jasmonate

If overall speculative role is
true, where, when and which cells
should synthesize brassinosteroids?

If BR is really a messenger in the GA action sequence or vice versa, their levels should rise and fall together.

Darkened plants should have high levels of BR, well lighted plants, low levels. Like abundance signals BR may be mostly made in meristematic cells and much less so as cells mature. (Or for real theoretical beauty, deficiency hormones should be made mostly in mature cells and much less so in meristematic cells). BR should be made when a cell has less than enough sugar to support both it any cell dependent on it for sugar acquisition. Thus BR is an indication that sugar exists in less than enough amounts to continue the plant at its current size, thus the plant must use emergency stores of starch, find new sources of the molecule and cut down on its sinks.

If overall speculative role is
true, what should exogenous
brassinosteroid treatment produce?

High levels of exogenously applied BR should induce JA synthesis, because many of BR's effects may be to increase sugar levels within the plant, if only temporarily. This may include making dormant reactions that normally depend on sugar.

If overall speculative role is true, what
should brassinosteroid inhibit and stimulate?

BR should encourage shoot and new shoot growth, but inhibit root growth and even encourage root senescence. This may be a particularly apparent when ethylene levels are high and strigolactone and ABA levels are low and levels low as this is an indication that resources need to rerouted from the root to the shoot and ABA levels are low and levels low as this is an indication that resources need to rerouted from the root to the shoot.

If overall speculative role is true, how
should brassinosteroid affect storage?

BR should cause the emptying of stored sugar reserves found in vacuoles or tubers.

If overall speculative role is true, how
should brassinosteroid be transported?

Sugar deficiency, on average should be detected in the roots first, the point furthest from the source of sugar. BR may be transported from the roots to the shoots where presumably they repel sugar and send it in the opposite direction back to the low sugar roots.

If overall speculative role is true, how should
brassinosteroid affect attraction and repulsion?

BR should generally push all nutrients and abundance signals/hormones out of cells. BR should attract the deficiency signals/hormones, ABA, ET and strigolactones, leading to positive feedback and cell senescence. BR should perhaps also work with JA to attract nutrients and positive hormones to leaves that are making jasmonic acid and thus are efficient synthesizers of sugar.

If overall speculative role is true, how should brassinosteroid affect apical dominance?

BR should break shoot apical dominance because low sugar levels are an indication of poor performance by the currently dominant apical shoot. BR may strengthen the currently dominant root apices in order not to encourage any new root growth which would be a further sink on sugar levels.

If overall speculative role is true, how
should brassinosteroid affect Cell Division?

Although it may encourage cell division in the shoots, if it is inducing new ones, BR should generally inhibit cell division, as a sugar deficient plant is in no condition to expand.

If overall speculative role is true, how should brassinosteroid affect senescence?

Just as I am hypothesizing that SA, JA, IAA and CK all need to be present to induce cell division, ABA, GA/BR, ET and strigolactone may all need to be present for cell senescence to proceed. may all need to be present for cell senescence to proceed. BR should encourage senescence, particularly of root tissue whose nutrients can be cannibalized and used to make more sugar producing shoot and leaf tissue.

If overall speculative role is true, how should brassinosteroid effect growth directions to provide balance in the plant?

BR should lengthen leaves and stems like GA. Presumably stem lengthening accomplishes moving shaded plants back into the sunlight.

Proven Synthesis and Transport

"One well-supported hypothesis is that all tissues produce BRs, since BR biosynthetic and signal transduction genes are expressed in a wide range of plant organs, and short-distance activity of the hormones also supports this." 96 97 Why this makes sense - GA may be made in just meristematic or for more theoretic beauty, in just senescent cells. Whereas GA is transported all over the plant and acts locally through BR.

BR is transported acropetally (upward). Why this makes sense - Sugar deficiencies are detected in the root and transported to act in the shoot.

Proven Effects

Promotes epinasty through synthesis of ethylene. Why this makes sense - GA/BR initially causes the release of stored sugar which increases metabolism, using up oxygen and causing rises in ethylene.

BR inhibits leaf abscission . Why this makes sense - BR being part of the sugar deficiency signal, would like to preserve as many apparatuses of sugar synthesis (leaves) as it can.

Plants found deficient in brassinolides suffer from dwarfism. Why this makes sense - is part of the same pathway that produces dwarfism in gibberellin mutants. GA/BR is probably used by a plant to lengthen it's stem during dark periods, fueled by dissolving of stored starch.

"Promotes cell expansion and cell elongation; works with auxin to do so." Why this makes sense - BR's complement is jasmonates which presumably initiates cell and tissue broadening. BR mirrors gibberellin's broadening.

"Acceleration of senescence in dying tissue cultured cells; delayed senescence in BR mutants supports that this action may be biologically relevant." Why this makes sense - presumably tissue already slated to senescence is in the positive feedback loop discussed previously as existing for all deficiency hormones once beyond hibernation "valley" levels.

BR- Provides protection to plants during chilling and drought stress. Why this makes sense - BR presumably initially frees up stored sugar which allows for greater metabolism which itself liberates heat and water.

Low levels of BR promotes root lengthening independent of auxin and ethylene. 51 Why this makes sense - the release of stored starch may temporarily allow for the release of root growth if it is limited by sugar levels.

Higher BR levels inhibits root growth. Why this makes sense - a plant facing sugar deficiencies need to inhibit root growth.

Promote apical dominance. Why this makes sense - a plant facing sugar shortages is probably in need of bolting or rapidly getting higher and punching through shade into sunlight again, by investing heavily in the lengthening of the current apical meristem. Granted, you could also argue that it should allow for other apical meristems to be given a try as the current one is unsuccessful and leading to sugar deficiencies...

Enhances seed germination although apparently not by the same pathway as GA. Why this makes sense - ? just as GA enhances seed germination BR should also, by releasing stored starches found in the seed. This conflict may be resolved later or perhaps has already been resolved. Of course I'm probably oversimplifying in this whole effort too.

Promotion of vascular differentiation; BR signal transduction has been studied during vascular differentiation. Why this makes sense - xylem differentiation doesn't make too much sense, but phloem differentiation would bring needed sugar down to sugar deficient roots.

"Inflorescences treated with brassinolide alone had no effect on ethylene production. However, when brassinolide was used in combination with IAA there was a dramatic increase in ethylene production above the induction promoted by IAA alone." Why this makes sense - IAA causes increases in respiration as it is an indicator of oxygen surplus. Once ethylene is produced, it starts pushing out nutrients. Adding BR is like adding fuel to the fire and leads to a climacteric export of all nutrients including oxygen thus leading to an even greater evolution of ethylene.

Brassinolide

Natural steroid found in plants.
Promotes cell elongation and division in plants.
It helps in increasing the percentage of fruit setting.
Regulates differentiation in tissue culture.
When applied during flowering stage, can decrease the chances of flower dropping and fruit dropping.
Improves the plant's ability to deal with diseases.
Improves the growth of the germinating seed.
Can be used in drench or foliar feed applications.
Strengthens a plant's immunity to stresses such as drought, salinity and cold.
Is an important element for plant growth and helps increase yield.


0.1% Brassinolide Specification:

Product Name : 24-Epibrassinolide - Brassinolide - BRASS - BL
Cas No: [78821-43-9]
Structure Formula : C28H48O6
Molecular Weight 480.68
Appearance: White crystals
Purity: 0.1%
Melting point: 254-256°C

Usage of 0.1% Brassinolide:

Brassinolide is fully water soluble.
Can be used in the germination of seeds, or propagation of clones.
Can be used in the vegetative growth or flower stages.
Can be used in drench feeds, hydroponic systems, soil, coco, soilless mediums, and foliar sprays.


Disclaimer:
This is Dependant on timing - Strain - Other Hormones used
 
Last edited:

shaggyballs

Active member
Veteran
oligosaccharins

Oligosaccharins are carbohydrate fragments that consist of short, branched chains of sugar molecules. Some trigger the production of phytoalexins, which are anti-microbial compounds that limit the spread of plant pathogens. Other oligosaccharins inhibit flowering and induce vegatative growth. They may function overall in cell growth and development.

Degradation of cell walls can result in the production of biologically active fragments 10 to 15 residues long, called oligosaccharins, that may be involved in natural developmental responses and in defense responses. Some of the reported physiological and developmental effects of oligosaccharins include stimulation of phytoalexin synthesis, oxidative bursts, ethylene synthesis, membrane depolarization, changes in cytoplasmic calcium, induced synthesis of pathogen-related proteins such as chitinase and glucanase, other systemic and local “wound” signals, and alterations in the growth and morphogenesis of isolated tissue samples.

The best-studied examples are oligosaccharide elicitors produced during pathogen invasion .
For example, the oomycete Phytophthora secretes an endopolygalacturonase (a type of pectinase) during its attack on plant tissues.
As this enzyme degrades the pectin component of the plant cell wall, it produces pectin fragments—oligogalacturonans—that elicit multiple defense responses by the plant cell.
The oligogalacturonans that are 10 to 13 residues long are most active in eliciting these responses.



Scheme for the production of oligosaccharins during fungal or oomycete invasion of plant cells. Enzymes secreted by the plant, such as chitinase and glucanase, attack the fungal or oomycete wall, releasing oligosaccharins that elicit the production of defense compounds (phytoalexins) in the plant. Similarly, fungal or oomycete pectinase releases biologically active oligosaccharins from the plant cell wall. Fungal, but not oomycete, walls contain chitin.

Plant cell walls also contain a (1,3)-β-D-glucanase that attacks the (1,3)-β-D-glucan that is major component of oomycete but not most plant cell walls. When this enzyme attacks the oomycete wall, it releases glucan oligomers with potent elicitor activity. The wall components serve in this case as part of a sensitive system for the detection of pathogen invasion.

Plants and microbes also possess inhibitory proteins that block the activity of the each other’s degradative enzymes . For example, plants have inhibitory proteins that inhibit or otherwise modify the activity of microbial (but not plant) polygalacturonases, glucanases, and xylanases, presumably to thwart microbial attacks. A similar trick is played out by some plant pathogens, which secrete proteins that inhibit plant defense enzymes.
 

shaggyballs

Active member
Veteran
Jasmonates

Speculative Overall Role

Sugar abundance signal

Growth Direction Tendencies are Broadening or widening
What is jasmonic acid's speculative
complementary deficiency signal?

Gibberellin/Brassinosteroid

If overall speculative role is
true, where, when and which
cells should synthesize jasmonate?

If the speculations are true, it would suggest jasmonic acid would be made more in the shoots than the roots. The finding that wounding causes the release of Jasmonic acid might be explained in terms of a rise in intercellular sugar due to ruptured cell contents releasing sugar and catabolic enzymes which would further break down cellulose and other sugar containing molecules.

If overall speculative role is true, what should exogenous jasmonate treatment produce?

Should induce GA, because JA up regulates various processes limited by sugar levels. Exogenously applying JA leads the plant to falsely believe that it has high levels of sugar, thus engaging all sorts of reactions that use sugar, thus further depleting what may simply be a homeostatic level of existing sugar and moving this level into the deficiency range.

If overall speculative role is true, what
should jasmonate inhibit and stimulate?

Should Induces new root growth, just like auxin. If auxin is also present, JA should inhibit shoot growth because high JA and IAA levels are an indication of at least a short term lack of need to expand the shoots.

If overall speculative role is true,
how should jasmonate affect storage?

Should cause sugar to be stored in proteins and tubers for less propitious times.

If overall speculative role is true,
how should jasmonate be transported?

May be expected to travel in the direction of the roots, away from the shoots and particularly the shoot meristems. Regions of a cell or tissue or plant part that contains high JA, may particularly attract sugar and transport of sugar may follow active JA transport down a plant.

If overall speculative role is true, how should
jasmonate affect attraction and repulsion?

Should attract all nutrients and abundance signals to a cell and repulse deficiency signals.

If overall speculative role is true, how
should jasmonate affect apical dominance?

Should induce shoot apical dominance along with auxin, however the possibility exists for two dominant apices if one is particularly good at sugar production (in the light) and one good at oxygen harvesting (in the wind). May break root apical dominances under conditions of low CK and SA.

If overall speculative role is true, how
should jasmonate affect Cell Division?

Is actually necessary for cell division along with auxin, cytokinin and Salicylic acid. If there are some plant callus lines that will divide with only auxin and cytokinin present it is because these cell lines are mutants that produce SA and JA natively, or these other hormones are unknowingly being included with the "other" nutrients/vitamins that are also added to calluses to get them to divide.

If overall speculative role is true, how
should jasmonate affect senescence?

Should protect plant tissue from senescence, particularly root tissue.

If overall speculative role is true,
how should jasmonate effect growth
directions to provide balance in the plant?

Because ET and IAA show complementary growth patterns with ET broadening and IAA lengthening and the same is true for CK (broadening) and BR (lengthening), we might expect that JA should show a complementary growth pattern to GA's cell lengthening, thus JA should broaden cells and plant tissue.

Proven Synthesis and Transport

JA exist at high levels in flowers and developing pericarps. Why this makes sense - flowers have high amounts of sugar available in order to produce nectar.
JA exist at high levels in the chloroplasts of illuminated plants. Why this makes sense - chloroplast have high amounts of sugar due to photosynthesis.
JA increases in response to mechanical stress and produce tendril coiling. Why this makes sense - ?? mechanical stress damages cell walls releasing cell contents high in sugar and enzymes that catabolize cellulose? The plant then uses the following jasmonate rise as a symptom needing the response to mechanical stress it normally provides.
Jasmonate is made in response to wounding. 15 Why this makes sense - bruising and wounding ruptures cells and releases vacuole sequestered sugars. Also neighboring plant cell reaction to wounding may be to release amylases (by inducing GA?) which increases sugar levels in the inter cell spaces.
Jasmonates levels increase along with those of ABA under desiccation conditions. 19 Why this makes sense - since photosynthesis uses up water and so we'd expect photosynthesis to go down under desiccation, so instead this is the opposite of what the theory predicts. Perhaps the water loss countering measures ABA does in this experiment are enough to actually provide a boost to photosynthesis above the starting level because the amount of water available was a limiting factor.

That being said, excess photosynthesis will cause desiccation for the same reason, so a rise in jasmonate will eventually show a rise in ABA because the process of water use by photosynthesis is tied to its shortage in the plant. However jasmonate should show up then desiccation and then ABA, not in the order suggested by the finding.

Proven Effects

JA is involved in the tuber storage proteins system and a derivative may stimulate tuber formation. 16 17 Why this makes sense - storage proteins and tubers are induced by JA in order to store excess sugar.
JA induces chlorosis inhibits photosynthesis gene transcription.
Why this makes sense - chlorosis induced by JA, is a negative feedback loop to cannibalize excess photosynthesis machinery.
JA is an indication of excess photosynthesis capacity.
What JA does in flower and fruits is unknown, but it may be involved in the converting green leaf cells contents into seed storage proteins, carotenoid and the sugars.
Why this makes sense - fruits and developing seeds may use JA as a signal to stimulate the leaves to send sugar their way and to turn the sugar stream into stored starch.
JA and ethylene appear to act in tandem to enact plant defense response. Why this makes sense - ?
 

shaggyballs

Active member
Veteran
Jasmonates

Jasmonates are a small group of related molecules derived from linolenic acid. The first to be identified was isolated from the oil of Jasminum officinale, the Poet's or Common Jasmine. This vine — the national flower of Pakistan — is grown as an ornamental along the southern tier of the United States and the coast of California.

The most abundant member of the group is jasmonic acid (right).
Jasmonates are produced in several parts of the plant and travel in the phloem to other parts where they turn on (or repress as the case may be) gene expression. They bind to the promoters of their gene targets.

Jasmonates, like most of the other plant hormones, are implicated in a bewildering variety of functions. In one species or another, they
promote the ripening of fruit (perhaps working upstream of ethylene)
are needed for the production of viable pollen
drive the coiling of tendrils
inhibit root growth
affect seed germination
promote the development and opening of flowers
promote the secretion of nectar in flowers
Some of these functions have been demonstrated by the application of jasmonates to the plant and may not present an accurate picture of the role played by the jasmonates produced within the plant itself.

One function that is clearly mediated by endogenous jasmonate synthesis and translocation is the plant's response to damage, for example, by herbivorous insects feeding on it or by pathogens (e.g. fungi) invading it. In this case the response is to turn on the expression of genes that encode a variety of defenses against the damaging agent.

JasmonicAcid.png


Methyl Jasmonate (MeJa)

Spurr says:
Jasmonates (as methyl ester of jasomic acid [MeJA], aka methyl jasomate, jasomonic acid [JA] or methyl dihydrojasmonate [MDHJ]):

MeJA increases glandular trichome density (over X leaf area) and number (total trichs); as well as being evidenced to increase terpenoid content. Salicylic acid (i.e. Advanced Nutrients 'Scorpion', or the analog aspirin) that is used to induce SAR (Systemic Acquired Resistance), hinders trichome density and number and has "negative cross-talk" to jasmonates, i.e. it hinders some jasmonate actions.

There is some evidence that brassinosteroids and jasmonic acid also have negative cross-talk, thus I apply methyl jasmonic acid alone (i.e., methyl easter of jasomic acid), and only in pre-flowering. I apply it as 100 ppm, but 50 ppm is also good and I am testing at lower ppm soon, e.g., 10 ppm and 25 ppm (lower is better if the same result is found).

Jaz Spray:


It contains methyl dihydrojasmonate (MDHJ), has a similar effect to methyl jasmonic acid (MeJA). However, using methyl jasmonic acid (aka methyl jasmonate) is preferable for increasing glandular trichome density (X trichs over Y area). If my quickly done math is correct, application rate as suggested on bottle (45 ml per quart, with 0.68% MDHJ (w/w) in 453.6 gram bottle that has a volume of 473 ml), the ppm is ~300-310 (depending upon molar mass of MDHJ).
http://www.jazsprays.com/Jaz-Rose-Sp...trate_p_8.html

"METHYL JASMONATE APPLICATION INDUCES INCREASED DENSITIES OF GLANDULAR TRICHOMES ON TOMATO, Lycopersicon esculentum"
ANTHONY J. BOUGHTON,* KELLI HOOVER, and GARY W. FELTON
Journal of Chemical Ecology, Vol. 31, No. 9, September 2005
Note, type IV glandular trichomes are defined as: "short with a 2-4 celled glandular head"



shag says:
My quick view:
I have only used Jaz spray!
Makes no taste weed acquire a taste.
Makes no smell weed acquire a smell.
Weed with a good taste already will share a common taste with anything Jaz is used on!
I would swear when taking cuttings and removing lower branches the other day I smelled the exact same smell!!(believe it or not)

I personally don't recommend jaz for MJ but I am interested in other forms.
 
Last edited:

shaggyballs

Active member
Veteran


Learn how to say Strigolactone correctly in English with this tutorial pronunciation video.

Strigolactones: A New Branching Hormone

Strigolactones are a group of terpenoid lactones that act as a host-derived signal in the rhizosphere communication of plants with arbuscular mycorrhiza and root weeds. They also occur as endogenous plant hormones regulating shoot branching in plants. All natural strigolactones contain a tricyclic ring system connected to a butenolide via an enol ether bridge. Most of the germination stimulants identified so far are strigolactones.

Shoot branches grow from axillary buds that arise in leaf axils. Auxin and cytokinin have long been known to be important plant hormones involved in regulating the outgrowth of axillary buds into branches. Recently, thanks to the use of branching mutants in several species, we now know the identity of a third hormone group, strigolactones, involved in this process.

http://5e.plantphys.net/article.php?ch=&id=486

1200px-Strigolactones_general_chemical_structure.png


Strigolactones:

Speculative Overall Role

Root nutrition other than water deficiency signal

Growth Direction Tendencies are Lengthening or elongating?
What is the speculative complementary stimulating hormone to strigolactones?

Cytokinin

If overall speculative role is true, where, when and which
cells should synthesize strigolactones?

Strigolactones should be made by root cells that don't have more than enough minerals to support both it and a dependent shoot cell. A shoot cell will make strigolactones if the mineral level dips below that necessary for continued life at its current size.

If overall speculative role is true, what should exogenous strigolactones treatment produce?

Exogenously applied strigolactones should prevent stem branching and encourage root branching. It should inhibit root senescence and encourage leaf senescence.

If overall speculative role is true, what
should strigolactones inhibit and stimulate?

Strigolactones should encourage root and new root growth, but inhibit shoot growth and even encourage shoot and leaf senescence.

If overall speculative role is true,
how should strigolactones affect storage?

Strigolactones should allow for the use of stored mineral stockpiles wherever they are located.

If overall speculative role is true, how should strigolactones be transported?

Strigolactones should be synthesized in the greatest amount in the section of the plant where mineral deficiency should show up first, which is the shoots. Strigolactones should then be tr4ansported to the roots to try to rectify the issue.

If overall speculative role is true, how should strigolactones affect attraction and repulsion?

Should repel all nutrients and abundance hormones/signals to a cell and attract deficiency hormones/signals.

If overall speculative role is true, how should strigolactones affect apical dominance?

Strigolactones should preserve shoot apical dominance and release root apical dominance allowing root branching.

If overall speculative role is true, how should strigolactones affect Cell Division?

Strigolactones should inhibit cell division.

If overall speculative role is true, how should strigolactones affect senescence?

Strigolactones should encourage senescence of shoot cells and tissues and inhibit senescence of root cells and tissues.

If overall speculative role is true, low should strigolactones effect growth directions to provide balance in the plant?

Strigolactones should complement cytokinin broadening of plant parts by causing lengthening of cells and tissues.

Proven Synthesis and Transport

Strigolactones control shoot branching. Why this makes sense - high SL levels suggest the need to conserve shoot growth because of short mineral supplies.

Synthesized mainly in the roots and in some parts of the stem. Why this makes sense - opposite of what is expected as usually deficiency hormones are synthesize in the tissue experiencing the shortage first, in this case the shoots.

Strigolactones are transported from the roots to shoots. Why this makes sense - see #2.

Strigolactones Are Transported through the Xylem. Why this makes sense - see #2.

Synthesis of strigolactones is tightly tied to Phosphate levels. Why this makes sense - SLs are mineral deficiency signals.

Proven Effects

Auxin and SLs change each other’s levels. Why this makes sense - spare phosphate as indicated by SL, is needed for oxygen to be used in respiration??

SL up-regulates photosynthesis machinery. Why this makes sense - same as above. Plant would rather store sugar if it can't respire as much??

SL stimulates root hair growth with the help of auxin and ethylene. Why this makes sense - more root hairs absorb more minerals thus combating mineral shortages like phosphate.

SLs inhibit branching even in the absence of auxin as shown with decapitated and auxin mutants. Why this makes sense - ?

Strigolactones are a group of closely-related molecules synthesized by most plants (possibly using carotenoids as the starting material).


Dizzlekush says:
Strigolactones initiate germination of AM, increase mitochondrial activity and density of AM, increase cell proliferation of AM (growth), and promote pre-symbiotic branching of AM. This naturally occurs in the rhizosphere as a/the plant starts lacking nitrogen and/or phosphorous and exudes specific strigolactones into the rhizosphere, or when certain environmental cues happen. The entire process usually unfurls in a 4-6 week period. One could essentially sidestep this whole 4-6 week natural forming of symbiosis by doing this process yourself, as i previously mentioned, saving your plants 4-6 weeks of work/waiting...

Again this is all just theory, im not aware of strigolactones ever being concentrated or synthesized and utilized in any sort of experimentation. We're pretty slow when it comes to strigolactone research ATM. We've known about them for over 15 years and have thought they were detrimental to plant growth for more than half the time we've been aware of them (because they were exuded by witches weed). Only ~7 years ago we discovered that they had beneficial aspects , and only 4 years ago did we find out that they are one of the essential groups of phytohormones in all (terrestrial at least) plants.

Master hormone controls plant growth

A single hormone co-ordinates how a plant grows in response to the environment, researchers have found.

Plant molecular biologist Dr Phil Brewer, of the University of Queensland, and colleagues, report their findings about a chemical called strigolactone

Stem thickening

Brewer and colleages have found that when strigolactone levels are high, not only does this stop buds from turning into branches, but it also thickens up the main stem.

This makes sure that a plant growing tall to reach the light, also has the structural strength to do so.

"We now think that this is a hormone that co-ordinates a response for the whole plant," says Brewer. "It's not just about the branching, it's also about other parts of the plant. It's about optimising its growth."

He says that for many years, scientists thought the thickening of stems was controlled by a chemical called auxin, but these latest findings challenge this.

"This is a breakthrough for us because it shows that auxin works through strigolactones to do this job," says Brewer. "It's a big change in the dogma of the field."

Brewer says he and collaborators are also finding strigolactone influences other parts of the plant too.

When nutrient levels are low, strigolactone levels rise and this stimulates production of root hairs and beneficial mycorrhizal fungi, which both help increase uptake of nutrients.

On the downside, some parasitic weeds have hijacked this system, says Brewer.

Strigolactone exuded from the plant roots signals to the seeds of these weeds its time to germinate and invade the nearby host plant.

Brewer says it's possible that strigolactone could be fed to trees that are being grown for timber to make them grow strong, tall and straight.

"It would also potentially make the trees more efficient at taking up nutrients,
http://www.abc.net.au/science/articles/2011/11/29/3378297.htm

Strigolactones fine-tune the root system
https://www.google.com/url?sa=t&rct...=D66T-r2Atjnm6gAOSouLYw&bvm=bv.57799294,d.b2I

Strigolactones

Strigolactones are a group of closely-related molecules synthesized by most plants (possibly using carotenoids as the starting material).

This is the molecular structure of one of them.


Strigolactones are manufactured in the roots and have been known for some time to
affect the germination of some plant seeds signal mycorrhizal fungi to connect to the root system forming a mutualistic relationship.
However, these activities do not qualify them as plant hormones (both activities take place in the soil surrounding the roots). Only if it can be demonstrated that strigolactones are translocated in the plant from the place of manufacture (roots) to another part of the plant where they exert an effect, can they be called hormones.



Two reports in the 11 September 2008 issue of Nature come close to proving the case.

Strigolactones (or possibly molecules derived from them) suppress the development of lateral buds and thus inhibit branching of the plant. Mutations in genes needed for the synthesis of strigolactones stimulate the development of lateral buds producing a more highly-branched plant than normal. Application of a synthetic strigolactone near the base of these mutant plants inhibits development of lateral buds above and thus restores normal branching.



Auxin and, in certain circumstances, abscisic acid also inhibit branching, that is, they promote apical dominance. But both auxin and abscisic acid participate in a number of different plant functions while the effect of strigolactones on branching seems quite specific.
 

shaggyballs

Active member
Veteran
Triacontanol

spurr says

a) One can dissolve 1 mg TRIA into 1 g Tween 20 at 90'C (194'F) in 15 minutes; and 10 mg of TRIA can be dissolved into 1 liter of water (albeit not without a lot of mixing and use of an emulsifier). Using chloroform is the best organic solvent for dissolving TRIA, but chloroform is hard to buy and thus I think is out of the question for most people here. So I am going to try using Tween 20 (see below). In the past I used Tween 20 (and Therm-X 70) mixed into very hot water with a blender to dissolve TRIA from super-grow; but that was messy (foamy); I used too much Tween 20...

b) the most common usage rates of TRIA in plant studies is 10^-4 M, 10^-5 M, 10^-6 M, 10^-7 M and 10^-8 M; that equates to ~43.88 ppm, ~4.38 ppm, ~0.438 ppm, ~0.044 ppm, ~0.004 ppm. The only info about TRIA and cananbis cited 1 ppm as effective dose rate. Most studies that used 10^-6 M, and other molarity concentrations, found 10^-6 M (i.e,. ~0.438 ppm TRIA) to be most effective. And 10^-4 M was found to hinder plant physiology in all studies I found. Some studies reported concentration by ppm, ex., 1 ppm, 2 ppm, 5 ppm, 10 ppm and 15 ppm; but most studies use Molarity (i.e., mol/L) for reporting concentration used.

c) I have used TRIA at ~25 ppm and ~10 ppm. I didn't notice a difference between both concentrations but less is always better for the same (or better) result. I have read of other people using 10 ppm and 25 ppm TRIA on cannabis with good results, too.

d) This next grow I plan to use 10^-6 M TRIA (i.e., ~0.438 ppm) instead of what I planned to use: 1 ppm. I think the result might be better with less TRIA (e.g., < 1 ppm), than with more TRIA (e.g., > 5 ppm).

e) I can post lots of studies if people wish to read them.


Waring: I have not tried this method yet, but it's sound and should work and requires no organic solvents. This method also includes a non-ionic surfactant so the mix is ready to spray on plants once diluted. FWIW, at least one patent I read suggests adding 2% (vol) canola oil (or rapeseed oil) to increase absorption of TRIA into leaf.

Background:

Below is the math I used to find ppm from molarity, as well as directions for making stock solution and then dilution of stock solution for ~0.438 ppm foliar spray in 1 liter of water. I didn't include the math I used to find the molecular weight of TRIA; but what I listed below is correct to the last decimal place (I didn't round).

In the info below I provide the 'how to' for 98% pure TRIA and for 85% pure TRIA. I provided both purities because the TRIA sold from chemical companies is 98% pure and the TRIA sold by super-grow is 85% pure. I was told super-grow will not re-open, but I assumed some people might have their TRIA, as I do. I plan to order 98% pure TRIA soon because my TRIA from super-grow is a bit old.




The salt that has been tested with TRIA that shows the most benefits is Calcium
Chloride. Out of all the cations, Calcium (+2) and Lanthanum (+3) had the most
synergy with TRIA, Ca (and Mg) being the least phytotoxic out of all tested. Out
of the Calcium salts, CaCl2 is the most tested salt, helps keep the solution at
a pH >7.0 (where TRIA is effective), and sterilizes the working solution. when
CaCl was added to the TRIA solution, yield enhancement is often tripled. It has
also been shown that these cations cannot be chelated if cation-TRIA synergy is
desired, which requires polysorbates (such as Tween 20) and some other non-ionic
surfactants to not be used in the formulation, as some non-ionic surfactants
will chelate the cations. Instead the formulation requires a polar organic
solvent such as alcohols, glycols, ketones, dipolar aprotic solvents etc. to
emulsify the solution (acetone seems to be the #1 choice). The above type of
formulation with TRIA being co-applied with a cation with a valence of +2 or
greater and the use of an organic polar solvent (and often one or more of
cytokinins, gibberellins and NAA) has shown to have greater improvements in
growth over TRIA formulations where a non-ionic surfactant has been used.
furthermore addition of any of the polysorbates have shown to have either
negative or no effects on TRIA applications.

while this is somewhat disappointing, research also shows that applying these
cations with a valence of +2 or greater to the soil in much greater quantities (in
comparison to foliage application) before TRIA application has a similar effect
to foliar co-applications of the cations with TRIA. so a feed heavy in Ca+ (and
most likely Mg, Mn, and Zn) a day or 2 before a TRIA application will be
beneficial if non-chelated Ca cannot be added to spray solution.

TRIA can be co-applied with auxins (aside from IAA, and not when combined with
Ca+ as Ca inhibits auxin activity), brassinosteroids, cytokinins, or
gibberellins. Oddly enough IAA has shown to have inhibitive effects on TRIA,
while other auxins (specifically synthetic ones) have shown no such relationship.
when i learn more of the mechanics behind this i will post it. Since Vitazyme is
a formulation with both Triacontanol and IAA in it, i would not suggest using
that product for optimum results. i personally do not suggest co-application
with auxins or gibberellins for most marijuana growing situations.
Brassinosteroids seem to have the least synergy with TRIA out of all
phytohormones tested, so i suggest co-appling TRIA with BAP or Ascophyllum
nodosum extract and separately applying Brassinosteroids in conjunction with a
non ionic surfactant.

U.S. Patent # 4470840

Quote:
During the course of research leading to the present invention, it has been
discovered, surprisingly, that auxins and other plant growth substances alter
the effects of 1-triacontanol. More specifically, the naturally-occurring auxin,
indole-3-acetic acid (IAA) has been found to counteract any growth-promoting
effect of 1-triacontanol. Auxins and 1-triacontanol are normally considered
plant growth stimulating agents, and the investigation into the inhibitory
interaction between the two substances led to the discovery that metal ions
having a positive valence of +2 or more not only reverse the inhibition, but
have an unexpected synergistic effect on the growth-stimulating effect of 1-triacontanol.
Furthermore, this effect occurs in the presence of free metal ions which are not
complexed or chelated. For example, the addition of surfactants such as Tweens,
which effectively complex the metal ions, show either a decrease in plant growth
when combined with 1-triacontanol formulations containing metal ions or show no
effect at all. This same effect may be observed using the formulations disclosed
in the U.S. Pat. No. 4,169,716 by Ashmead which teaches that 1-triacontanol may
show a synergistic effect when combined with certain metal proteinates and a
variety of other plant growth substances....
While the metal ions of the Hofmeister series having a valence of +2 or more are
known to effect auxin binding and are very effective in producing a synergistic
effect when combined with 1-triacontanol using the methods of the present
invention, other metal ions such as zinc, lead, cadmium, etc. are effective and
in some cases superior to the Hofmeister series metal ions. Since these other
metal ions are useful and are not known to affect auxin binding, the synergistic
effect observed in combination with 1-triacontanol may not be related to
increase auxin binding. Furthermore, since the pH of the formulations of the
present invention must be maintained over 7, auxin binding would necessarily be
inhibited rather than promoted (see Plant Physiol., 59: 357 1977)). Therefore,
no explanation for the surprising synergistic effect of metal ions having a
valence of +2 or more in the 1-triacontanol formulations is apparent.
Since surfactant additives or other additives which effectively complex the
metal ions of the present invention may not be used in carrying out the best
mode of the invention, research by the present inventor has led to the discovery
that the incorporation of a polar organic solvent must be used. The polar
organic solvent should be one in which 1-triacontanol is soluble to some extent,
and also one that shows a solubility in water. Such solvents are disclosed in U.S.
Ser. No. 47,696, filed June 12, 1979, and U.S. Ser. No. 146,005, filed May 2,
1980, both by the present inventor. The polar solvents of the present invention
include, but are in no way limited to, water soluble ketones, alcohols, ethers,
acids, amines, and dipolar aprotic solvents (such as dimethyl formamide,
dimethyl sulfoxide (DMSO), and hexamethyl phosphoramide), and the like.

patents that cover everything i've explained:
http://www.patents.com/us-4470840.html

U.S. Patent #4333758
http://www.freepatentsonline.com/4333758.html
 
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