How many plants must you select from to not be a "hack"

[VerdantGreen]

HAHAHAH!!! WOW! I learn something new everyday here at ICMAG I didn't know that songbird seed mixes had hemp seed in them that's crazy! Leave nature be damn government if the birds eat it in nature how you gonna try and ban the shit!!!! I swear this country is so backwards!!!!

that and hempseed used for fishing are 2 reasons why cannabis seed is legal in the UK

 

[Grat3fulh3ad]

Bottom line is If you dont have a lab to test THC/CBD your just spinnin your wheels and making a nice flower without documentation your a hack...yes I have a lab...and we test other folks stuff as well
Regards

I disagree, slightly. IMHO actual effects are better tested real world than as numbers.

But to carry your logic to it's conclusion... If you are not testing for every single terpinoid and flavinoid which can be shown to influence the effects of the THC/CBD present, or which has its own effect, then you must also be a hack.


IMHO, defining a hack would be more relative to how high the bar is set for their goals and how effectively those goals are met, not the specific methods used to get there.

I guess I'd rather be a hack selling seeds that grow plants that impress people, than a laboratory tech picking parents based solely on the concentration of thc/cbd. Most of the elite plants out there are not the result of a lab analyzed breeding strategy. To me basing a strategy on such limited criteria will result in a long list of mostly similar bland high hybrids.


per strain numbers are irrelevant to me, because I select plants not strains. I grow lots of 20-30 seeds all the time out of which zero get kept... sometimes I find something unique and impressive in a 12 plant run, or from a single seed... Selection begins at germination, every plant is constantly being judged all the way through it's life.

 

[GeneticsGoneMad]

Attitude is everything.....to a bragger... but Testing your results is factual Scientific Information...get with the program if you want to call yourself a breeder..Im on an F9 series now not f1 f2 or f3 8yrs + with one strain under development...Im not a kid and approach this plant like a true botanist would..

 

[Grat3fulh3ad]

LOL...
Carry on then, as will I.
all the best.

btw.
I approach the plant as someone who is truly in love with it would.
I did field work breeding seed corn for a large commercial seed company back in the early 90's.
Attitude I could care less about, it is results that matter.
I test all my results. Consumption tells me as much or more than your lab results.

and...

Im not a kid and approach this plant like a true botanist would..

Does a true botanist use the term recrossing to refer to generational line breeding?

Only time I figure recrossing applies is if I go across the street or the river and need to get back.

 

[Grat3fulh3ad]

get with the program if you want to call yourself a breeder...

I don't want to call myself a breeder.
I prefer Artistic Hybridization Engineer...

or Maybe... Hybridization Artist Creating Kind Seeds.

 

[VerdantGreen]

Attitude is everything.....to a bragger... but Testing your results is factual Scientific Information...get with the program if you want to call yourself a breeder..Im on an F9 series now not f1 f2 or f3 8yrs + with one strain under development...Im not a kid and approach this plant like a true botanist would..

so are you just developing a strain for drug companies to extract THC from? - if so you are on the right track im sure

if you are developing a strain for smokers then you might be barking up the wrong tree - time and time again i find that the strains people prefer are often not the most potent, but the ones with a desirable quality of high or smell or taste.

VG

 

[subrob]

Attitude is everything.....to a bragger... but Testing your results is factual Scientific Information...get with the program if you want to call yourself a breeder..Im on an F9 series now not f1 f2 or f3 8yrs + with one strain under development...Im not a kid and approach this plant like a true botanist would..

---see, this is why when you spammed our thread in the cali forums i wasnt sure if i should wish you good luck or not...haha...jury is still out....your pushing your biz hard, but you are not going to be able to pull off telling guys who have put out proven strains that they are not as good as you because they dont do things the same way as you...and i dont think you will be able to undermine consumers' confidence in said proven seedmakers just cuz they have not sent a sample and a cashiers check to your new business venture for testing....i am not jumpin in this conversation thinking i have anywhere near the base knowledge of at least a few people already in this thread, but i can smell another cali-goldrush business venture a mile away...and before you get offended, like i said, im not sure thats a bad thing...some of my bros have had these tests done on some of thier samples, and as many(with more knowledge than i) have said 27% thc doesnt mean its better...just thats its 27% thc...

 

[subrob]

I don't want to call myself a breeder.
I prefer Artistic Hybridization Engineer...

or Maybe... Hybridization Artist Creating Kind Seeds.

perfect!me, im a closet pollen chucker...maybe someday i will be a hack!
---good thread OP...And to kinda get back to the original subject...heres how i break it down in my limited experience:
STAGE1-POLLEN CHUCKING HACK....just like me for the last couple years...playing with the basics...learning the CRAFT..gettin lucky on a couple really nice, limited quantity hybrids...(which, appropriately get DONATED and not sold for MY profit)
STAGE2-SEEDMAKER....what i HOPE ive progressed into...got the basics down, making slightly more educated decisions on selection, getting a lil more stable results, understanding what to look for in males, able to isolate traits, sharing the responsibility to oother individuals w similiar interests and attitudes so we can work w a larger pool, together, and not have so many plants we draw extra attention... etc...but still MUCH left to learn.....the journeyman stage for those of us w a bluecollar background..i suppose, like a union job, this stage can last for a loooooong time depending on the desire, practices, and abilities of the individual.
STAGE3-BREEDER...well, not being one i cant tell you exactly what the requirements would be, but i suppose i will know when i get there, if i get there...though nowadays, as evidenced by quite a few of the seed companies out there, and some of the more popular ones at that, you can go from "why do my leaves go yellow at the end of flowering?" to master breeder in like, 6 years!
-----hows that sound to the peeps in here who know more than i? i know when people grow out seeds i made and refer to me as "the breeder" i always jump in and point out i am a chucker as i dont want ANYONE to think im elevating myself to any position i havent earned...and i dont want any real breeders jumpin my shit! haha

 

[Thundurkel]

I can dig it Subrob and agree with what you have to say and of course everything my good unaware of it maybe haha mentor Head who I pay attention to anytime he speaks on the subject and a few others around here...

 

[DocLeaf]

Still an interesting debate

 

[englishrick]

id just like to say,,,,,FULL RESPECT TO HEAD

but i still think ive got room to talk,,,,,,,,

all breeders have there place in our comunity,,,,,,EVEN HACKS,,,


THC is selected by nature,,,,,,<<<<we cant argue this point!!,,,,,,,nature gave us hemp,,,,hemp has sindromes,,,,within hemp populations plants with low THC% will be found,,,but the main point is that chemical THC is present!!! ,,,,HACKS and Breeders alike allready have a starting point...

evolutionary biology is a sub-field of biology concerned with the origin of species from a common descent and descent of species, as well as their change, multiplication and diversity over time.

the term "agent of selection" is used by evolutionary biologist`s to disscribe a form of enviromental pressure,,,,,this particular pressure has a dramatic impact on sucsessive gennerations and gives oppertunitys for rappid generation of novel superior genotypes....the supirior domesticates soon spread beyond there cradles of domestication into geographic areas with different enviroments,,,,,increeses in adaptedness within specific enviroments leads to still greater genetic differation among populations of domesticates

even a hack contibutes to the divercity of our culture!







nature offerd the opertunity but we domesticated it,,,now its are baby and what we know as good-weed could easly be lost in the wild

 

[arcticsun]

Ill need to add a comment to this GFH.. even tho I said I would leave the discussion.

Quote:Originally Posted by arcticsun
Mutations is a result of senescence, programmed habitat adaption following cell death.

Some mutation, you mean. There are many other specific stimuli which cause mutation.

There are several types of radiation which cause mutations
There are several chemicals which are mutagens
There are pathogens which are mutagens.

Pathogens, radiation and chemicals??? Im not seeing your point here, please elaborate. A radioactive environment should cause senescence .. sure.. What is your point?

Quote:
Its not a process that occurs accidentally. You will not get an affy genotype mutation in any habitat!

It is absolutely a process which occasionally occurs randomly.

There is nothing random about nature bro...


http://www.ias.ac.in/currsci/sep25/articles19.htm

Since senescence constitutes an internally regulated developmental process, it has a logic in plant life and therefore, carries significant physiological implications. A programmed senescence, is basically an adaptive mechanism and the death, its consequence, therefore, takes place on the organism’s own terms. In nature, senescence in leaves is the best example that fits into this concept. Leaf senescence has extensively been investigated in the last few years. The process, however, is not only concerned with death but involves several events associated with massive mobilization of nutrients in a highly ordered and regulated manner from senescing leaves to new leaves, developing fruits, seeds and buds, thus contributing to the nutrient cycling. The senescing leaves carry out these events and therefore remain viable and active. Although there are limits for generalization and extrapolation of the mechanism of leaf senescence in understanding the process in whole plants, the study however, provides vital clues to the knowledge of basics of senescence as a process.

Senescence of a leaf is temporally regulated in a co-ordinated manner1,2. The cellular components in the senescing leaves experience a sequential dismantling with a perfect order3,4. Although the process operates under the active control of genes, it is known to be modulated by environmental signals5. The precise triggering mechanism of leaf senescence still remains unclear but it is proposed to be induced by intrinsic and environmental factors5,6. In green leaves, the process is mostly characterized by a loss in total chlorophyll7. In addition, the degradation of macromolecules, namely proteins, nucleic acids, lipids and a decline in photosynthesis, remobilization of nutrients and the dismantling of cellular organelles are other major events associated with the process3,6. The genes regulating these events are known as senescence associated genes (SAGs)5,8. More than 30 SAGs are isolated, cloned and characterized in different plant systems.

Tell me what role or relevance radioactivity makes in plant physiology. What was said is somewhat weird and its thrown me off balance? I honestly dont understand your point.

Even if radioactivity causes mutations, its still senescence? There is no alternative process for radioactivity signals afaik? Please educate me on such if it exists.

There are no random mutations!

Thanks..

 

[Grat3fulh3ad]

lol... it is all random.
There are random mutations because some of the things which can cause mutation can occur as random events.

senescence |səˈnesəns|
noun Biology
the condition or process of deterioration with age.
• loss of a cell's power of division and growth.

Please tell me how heritable mutations all fit under this definition.
Tell me where your C&P'd article relates mutation to senescence.

senescence is most likely an epigenetic response is what the studies will eventually reveal, I'd wager heavily.


Mutation is rare and often random

 

[the_coota]

ill be doing an open pollenation with 30 LUI's, does that make me a hack?.. oh and what do i do with all the seeds!!? hahaha

EDIT: actually, the sheer fact that i dont know wot to do with the seeds im making prob does make me a hack imo

 

[Grat3fulh3ad]

...

Two classes of mutations are spontaneous mutations (molecular decay) and induced mutations caused by mutagens.


Spontaneous mutations on the molecular level can be caused by:

Tautomerism – A base is changed by the repositioning of a hydrogen atom, altering the hydrogen bonding pattern of that base resulting in incorrect base pairing during replication.

Depurination – Loss of a purine base (A or G) to form an apurinic site (AP site).

Deamination – Hydrolysis changes a normal base to an atypical base containing a keto group in place of the original amine group. Examples include C → U and A → HX (hypoxanthine), which can be corrected by DNA repair mechanisms; and 5MeC (5-methylcytosine) → T, which is less likely to be detected as a mutation because thymine is a normal DNA base.

Slipped strand mispairing - Denaturation of the new strand from the template during replication, followed by renaturation in a different spot ("slipping"). This can lead to insertions or deletions.




Induced mutations on the molecular level can be caused by:

Chemicals

Hydroxylamine NH2OH


Base analogs (e.g. BrdU)

Alkylating agents (e.g. N-ethyl-N-nitrosourea) These agents can mutate both replicating and non-replicating DNA. In contrast, a base analog can only mutate the DNA when the analog is incorporated in replicating the DNA. Each of these classes of chemical mutagens has certain effects that then lead to transitions, transversions, or deletions.

Agents that form DNA adducts (e.g. ochratoxin A metabolites)

DNA intercalating agents (e.g. ethidium bromide)

DNA crosslinkers

Oxidative damage

Nitrous acid converts amine groups on A and C to diazo groups, altering their hydrogen bonding patterns which leads to incorrect base pairing during replication.



Radiation

Ultraviolet radiation (nonionizing radiation). Two nucleotide bases in DNA – cytosine and thymine – are most vulnerable to radiation that can change their properties. UV light can induce adjacent pyrimidine bases in a DNA strand to become covalently joined as a pyrimidine dimer. UV radiation, particularly longer-wave UVA, can also cause oxidative damage to DNA[26].

Ionizing radiation


Viral infections

 

[Grat3fulh3ad]

It seems as though you have your chain of causality backwards... senescence seems likely the result of mutation, not the other way around.

http://www.springerlink.com/index/J636058Q4T68160T.pdf

Abstract Two evolutionary genetic models–mutation accumulation and antagonistic pleiotropy–have been proposed to explain the origin and maintenance of senescence. In this paper, we focus our attention on the mutation accumulation model. We re-examine previous evidence for mutation accumulation in light of new information from large-scale demographic experiments. After discussing evidence for the predictions that have been put forth from models of mutation accumulation, we discuss two critical issues at length. First, we discuss the possibility that classical fruit fly stock maintenance regimes may give rise to spurious results in selection studies of aging. Second, we consider evidence for the assumptions underlying evolutionary models of aging. These models assume that mutations act additively on age-specific survival rate, that there exist mutations whose effects are confined to late age-classes, and that all mutations have equal effects. Recent empirical evidence suggests that each of these three assumptions is unlikely to be true. On the basis of these results, we do not conclude that mutation accumulation is no longer a valid explanation for the evolution of aging. Rather, we suggest that we now need to begin developing more biologically realistic genetic models for the evolution of aging.

 

[arcticsun]

These models assume that mutations act additively on age-specific survival rate, that there exist mutations whose effects are confined to late age-classes, and that all mutations have equal effects. Recent empirical evidence suggests that each of these three assumptions is unlikely to be true. On the basis of these results, we do not conclude that mutation accumulation is no longer a valid explanation for the evolution of aging. Rather, we suggest that we now need to begin developing more biologically realistic genetic models for the evolution of aging.

You make that conclusion from the abstract you linked?

 

[Grat3fulh3ad]

No. The abstract I linked supports that conclusion, however.
I can provide more evidence that you have it backwards if you like...

 

[Grat3fulh3ad]

More abstracts which include the concept that senescence evolved as a result of accumulated mutations. Please show me one thing indicating that senescence is the primary cause of all mutation since you doubt my conclusions...

Laboratory experiments show us that the deleterious character of accumulated novel age-specific mutations is reduced and made less variable with increased age. While theories of aging predict that the frequency of deleterious mutations at mutation–selection equilibrium will increase with the mutation's age of effect, they do not account for these age-related changes in the distribution of de novo mutational effects. Furthermore, no model predicts why this dependence of mutational effects upon age exists. Because the nature of mutational distributions plays a critical role in shaping patterns of senescence, we need to develop aging theory that explains and incorporates these effects. Here we propose a model that explains the age dependency of mutational effects by extending Fisher's geometrical model of adaptation to include a temporal dimension. Using a combination of simple analytical arguments and simulations, we show that our model predicts age-specific mutational distributions that are consistent with observations from mutation-accumulation experiments. Simulations show us that these age-specific mutational effects may generate patterns of senescence at mutation–selection equilibrium that are consistent with observed demographic patterns that are otherwise difficult to explain.

Quantitative genetic approaches have been developed that allow researchers to determine which of two mechanisms, mutation accumulation (MA) or antagonistic pleiotropy (AP), best explain observed variation in patterns of senescence using classical quantitative genetic techniques. These include the creation of mutation accumulation lines, artificial selection experiments and the partitioning of genetic variances across age classes. This last strategy has received the lion's share of empirical attention. Models predict that inbreeding depression (ID), dominance variance and the variance among inbred line means will all increase with age under MA but not under those forms of AP that generate marginal overdominance. Here, we show that these measures are not, in fact, diagnostic of MA versus AP. In particular, the assumptions about the value of genetic parameters in existing AP models may be rather narrow, and often violated in reality. We argue that whenever ageing-related AP loci contribute to segregating genetic variation, polymorphism at these loci will be enhanced by genetic effects that will also cause ID and dominance variance to increase with age, effects also expected under the MA model of senescence. We suggest that the tests that seek to identify the relative contributions of AP and MA to the evolution of ageing by partitioning genetic variance components are likely to be too conservative to be of general value.

 

[BeAn]

Hacks are in it for the $$$£££, and dont care whether their beans are good or not, most of the time on the back of the...: pro's, with the means and the logic, then theres the entusiasts with the drive and passion but not the lab, then theres the seedmakers who think its fun to hit up girls with boys n grow the pips to smoke, then theres matey who didnt know the difference between the sexes n got like a million beans and is happy..for everyone else theres mastercard...