The determinator of sex

[xmobotx]

it might be better to say in 'between an old mobile phone and windows 3.1'

 

[Infinitesimal]

What everyone needs to be doing is thinking about these traits in terms of their evolutionary history and the advantages they may confer. There are a huge number of species which form either colonies of clones (I'm thinking heather) or exist in groups of individual plants - either way they are presumably going to be in close proximity to others of their kind. If one plant can tell others around that it's being munched on, its neighbours can prepare for that eventuality or what have you. The precise effect doesn't matter but there's an obvious advantage, it's just down to working out how/what happens.

LOL, just how does a plant prepare to get munched on? hehehe... can you feel the plants pain... can you feel their PAIN MAN?

you say stuff like that then act like I don't understand something

The problem there is that the group size is no where near large enough. If you want to actually determine if a value (m/f ratio) is being affected by the environment you need to be doing some sort of statistical analysis. The exact analysis method would be dependent on the number of/type of environmental factors you were controlling but it's a bit more complex than dividing 25 by 50.

lol, it was just a HYPOTHETICAL example... to make a point, not a scientific study to prove anything... you can extrapolate those numbers and the number of rooms to any scale you like and the results will be the same... its probabilities and luck of the draw... your shortsightedness is YOUR weakness

So how is this not an example of environment being capable of determining sex? As DP and I have both said, as females are capable of producing pollen it seems fairly apparent that the genes responsible for a 'male' phenotype are present in both males and females, as we would expect if the plant evolved from a monoecious ancestor fairly recently.

I am a little confused you keep bringing up females capable of producing pollen... are you referring to chemically treated females... environmentally stressed females or plants that are genetically both male and female????

... they are all different... but the fact that both chemically stressed females and environmentally stressed females progeny grow all female when not overly stressed... combined with the fact that genetic herms progeny produce more herms pretty much proves that it is controlled by the DNA.


and its not the same because I am saying... that the effects you are seeing are do to changes in the epigenome either environmentally or chemically stressing the plant using epigenetic triggers... which doesn't effect the DNA of which X and Y chromosomes are a part of.

(XX)(XY) mosaic hermaphrodites, which are not a function of the epigenome but the DNA (chromosomes)... have two different cells lines in their bodies some cells are (XX) and some cells are (XY) male... in humans they have both ovaries and testicles... and depending on their hormone levels may produce either sperm or eggs (or potentially both)

epigenetics allow for suppressed ancestral traits to be expressed through modifying the gene function through said chemical tags...

for instance, since birds evolved from dinosaurs... scientist postulate that using epigenetics it may be possible to reverse engineer species using their modern day living descendants... for instance using epigenetic to cause an emu to express traits that were present in its prehistoric ancestors because the descendants still maintain the basic genetic information and frame work of their ancestors...

No they don't; I have a feeling you may be confusing some of the ancestral traits we see in animal embryonic development or something with epigenetics. Epigenetics is likely involved but it's not a well understood field, don't make out like you know what you're talking about.

No, I understand embryonic development but I think the DNA similarities are responsible for most of that... but embryonic development had nothing to do with what I was saying.

No they don't; environment and genes have both changed. The proteins expressed by cells today have had an extra x million years to mutate. This includes both the epigenetic switches you speak of and the receptors that would be needed to recognize them and the enzyme pathways involved in processing them.

this is what I was talking about...

Atavism
From Wikipedia, the free encyclopedia



Atavism is the tendency to revert to ancestral type. In biology, an atavism is an evolutionary throwback, such as traits reappearing which had disappeared generations before.[2] Atavisms can occur in several ways. One way is when genes for previously existing phenotypical features are preserved in DNA, and these become expressed through a mutation that either knock out the overriding genes for the new traits or make the old traits override the new one. A number of traits can vary as a result of shortening of the fetal development of a trait (neoteny) or by prolongation of the same. In such a case, a shift in the time a trait is allowed to develop before it is fixed can bring forth an ancestral phenotype.[3]



Evolutionarily, traits that have disappeared phenotypically do not necessarily disappear from an organism's DNA. The gene sequence often remains, but is inactive. Such an unused gene may remain in the genome for many generations.[4] As long as the gene remains intact, a fault in the genetic control suppressing the gene can lead to it being expressed again. Sometimes, dormant genes can be induced to be expressed by artificial stimulation.

Examples observed include:
Hind legs on whales[2] or snakes
Hind fins on dolphins[2]
Extra toes on horses, as in archaic horses[5]
Re-emergence of sexual reproduction in the flowering plant Hieracium pilosella and the Crotoniidae family of mites. [6]
Teeth in chicken [7]

Examples in humans [edit]
Atavisms have been observed in humans as well. Babies have been born with a vestigial tail, called "coccygeal process", "coccygeal projection", and "caudal appendage".[2] It can also be evidenced in humans who possess large teeth, like those of other primates.[8] In addition, a case of "Snake Heart", the presence of "coronary circulation and myocardial architecture [which resemble] those of the reptilian heart", has also been reported in medical literature.[9]

http://www.merriam-webster.com/dictionary/atavism
atavism
Popularity


at·a·vism noun \ˈa-tə-ˌvi-zəm\

Definition of ATAVISM

1
a : recurrence in an organism of a trait or character typical of an ancestral form and usually due to genetic recombination
b : recurrence of or reversion to a past style, manner, outlook, approach, or activity <architectural atavism>
2
: one that manifests atavism : throwback


as far as scientist reverse engineering species using their modern descendants..

watch all four parts... they don't use the word Epigenetics but that is what they are talking about "turning on/off genes"

part 2
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part 3
[YOUTUBEIF]-B2c79tq-Do[/YOUTUBEIF]

part4
[YOUTUBEIF]L_Uiuy-lfGs[/YOUTUBEIF]

part 5
[YOUTUBEIF]v6vHdRfi14c[/YOUTUBEIF]

the point is... epigenetics can cause latent ancestral genes to express themselves...

again atavism... the genes are still there!

"mutate" you mean inherited... recombinant genetic pairing (in cannabis as in humans) results in "mutated" offspring... "mutated" meaning genetically different from either parent... since they receive half of the parents genetic material they are not identical copies and have mutated DNA... but the fact is after doing human genome studies we know that there are not enough genes in our DNA to account the variety of phenotypes... the differences between us are epigenetic... and epigenetic changes can be reversed by moving the chemical tags and turning the gene on or off

and if epigenetics doesn't allow for expression of latent ancestral traits then how do you explain the fact... that we share so much of our DNA with chimps but they resemble our primate ancestors so much more than we do... why is that?

are they expressing latent ancestral traits that have been suppressed in us Epigenetically?

blocking the ethylene likely triggers the expression of latent monoecious traits buried in the cannabis genome... or at least maybe?

Now that language is better Sorry to be an arse, people asserting 'facts' about brand new fields of biology that are far from being understood in relation to our understanding of other mechanisms within a cell. When you talk about epigenetics you have to remember that the term itself is as vague as can be. Talking about the epigenome is rather like talking about the proteome - the term itself simply mean above genetics so covers the changes in phenotypes which can occur without a change in genotype (as you said) however the way this is done varies massively and adds a layer of complexity to genetics which is just damn frightening to think about (I do). So let's look at a couple of ways in which genome expression is controlled briefly:

DNA Methylation - CpG islands in promotor regions of DNA are methylated by proteins. This prevents the binding of protein complexes required for the initiation of transcription and also leads to:

Histone Modification - Acetylation, phosphorylation, ubiquitination and the reverse reactions are possible on numerous sites of the histone depending on the constituent subunits. These can make some regions of DNA more or less accessible to transcription associated proteins or perhaps changes the affinity of said proteins for binding. Who knows? The point is that the number of modification variants means that every single nucleosome is likely to be completely unique in terms of it's modified structure.

siRNA - small interfering RNA, small single stranded pieces of RNA complimentary to sections of a specific mRNA or multiple RNAs. Double stranded RNA is recognized by RNAses for degredation so prevents expression unless a) [mRNA]>[siRNA] b) Somehow RNAase cannot detect it? c) The double stranded RNA has some other function we don't know about.

So say we have a defined pathway for the synthesis of a protein that forces a plant to be male (hypothetical here; obviously it's way more complex ), how readily to transcription factors bind to that gene? This can be varied greatly (almost in an analogue fashion due to histone modification and DNA methylation) which can lead to varying levels of the transcription of that gene into mRNA. We then have alternative splicing - how much of the 'male protein' mRNA is actually going to make it out and how many of those splice variants produce a completely different protein? At the same time and outside of the nucleus whilst these splice variants are floating around trying to find a ribosome, siRNA is present. How many siRNAs are capable of blocking these mRNA splice variants? And then of course we have to consider that each of these genes responsible for the synthesis of these siRNAs (genes don't just code proteins remember) are affected by exactly the same mechanisms described above. It gets so messy, convoluted and complex that you begin to loose hope of ever understanding how it all works.

ah ha, "completely unique in terms of it's MODIFIED structure"... so the unmodified genetic DNA structure is still there (evolution just builds off the structure) and Epigenetics is dynamic and can undo and redo modifications to the structure, using the chemical tags can turn on or off expression... hence again the genetic similarities between vastly different species and the ability for an individual (in this context cannabis) to express latent traits from its ancestral past, in this case a female plant that makes pollen.

those are all processes used in Epigenetic research that and PCR among others... I don't think Epigenetics is that vague; new sort of... relatively so, not well understood by many sure... I don't claim to be any expert in the field either just a curios person with an interest in and ability to learning... but I am not talking about causing intentional Epigenetic changes... I am saying that epigenetics can be used to explain some of these changes we see within an individual... (cannabis)

the mice... they can turn on or off the genes by feeding methyl rich food to trigger the gene that makes them fat

and 50% using trial epigenetic therapy drugs treating their cancer have gone into remission... by reactivating genes

[YOUTUBEIF]7WEHoCA1hpo[/YOUTUBEIF]

[YOUTUBEIF]ehwFVgQ82ZY[/YOUTUBEIF]

don't make out like you know what you're talking about.

maybe take your own advise ay?

 

[DemonPigeon]

And DP, you bugger, made me feel really old.

That's fine your threads sometimes make me feel stupid

Both examples prove no one likes the truth in a quantity larger than a pinch of salt


Btw is it me or can you feel a BioChem storm brewing? I'm going to put sandbags around my alleles and battern down the gametes.

 

[Infinitesimal]

DNA Methylation - CpG islands in promotor regions of DNA are methylated by proteins. This prevents the binding of protein complexes required for the initiation of transcription and also leads to:

Histone Modification - Acetylation, phosphorylation, ubiquitination and the reverse reactions are possible on numerous sites of the histone depending on the constituent subunits. These can make some regions of DNA more or less accessible to transcription associated proteins or perhaps changes the affinity of said proteins for binding. Who knows? The point is that the number of modification variants means that every single nucleosome is likely to be completely unique in terms of it's modified structure.

siRNA - small interfering RNA, small single stranded pieces of RNA complimentary to sections of a specific mRNA or multiple RNAs. Double stranded RNA is recognized by RNAses for degredation so prevents expression unless a) [mRNA]>[siRNA] b) Somehow RNAase cannot detect it? c) The double stranded RNA has some other function we don't know about.

So say we have a defined pathway for the synthesis of a protein that forces a plant to be male (hypothetical here; obviously it's way more complex ), how readily do transcription factors bind to that gene? This can be varied greatly (almost in an analogue fashion due to histone modification and DNA methylation) which can lead to varying levels of the transcription of that gene into mRNA. We then have alternative splicing - how much of the 'male protein' mRNA is actually going to make it out and how many of those splice variants produce a completely different protein? At the same time and outside of the nucleus whilst these splice variants are floating around trying to find a ribosome, siRNA is present. How many siRNAs are capable of blocking these mRNA splice variants? And then of course we have to consider that each of these genes responsible for the synthesis of these siRNAs (genes don't just code proteins remember) are affected by exactly the same mechanisms described above. It gets so messy, convoluted and complex that you begin to loose hope of ever understanding how it all works.

I don't know how any of that pertains to the intersex traits observed in cannabis???

but since you are sooooo smart, Riddle me this....

further more... please explain... as I think I have given an understandable basic explanation to the sexual controls of the cannabis plant and anyone refuting it should at least be able to do the same.

With that in mind,

What is the mode of action... what is happening inside the seed when you lower the temps, increase the humidity, decrease the wind, or whatever else... that is supposedly creating more or less males or females?


Peace,
Infi

 

[BullDogUK]

is it me or can you feel a BioChem storm brewing? I'm going to put sandbags around my alleles and battern down the gametes.

The power of Thor compels thee!

But anyway, a lot of points were raised so I feel I should go through them in order. As I said in the previous post, sorry if I came across as a bit arsey but we are no where near being close to understanding how genetics lead to changes in organism phenotype; there are still far too many blank spaces for the full picture to be apparent.

you're talking about sexual expression and complaining about determination. 2 separate things. Determination is genotype, expression is phenotype. Phenotype doesn't determine inheritance, genotype does.

Well I'm not too sure, if 'male' genes are present outside of the Y chromosome then it's rather pointless making that distinction as the difference would be entirely within the phenotypes and protein expression profiles of the plants. Saying that, the Y chromosome being a giant promoter/regulatory region is a wild guess so probably completely wrong Otherwise yeah, my bad, 3am posts are never the most thought out >.<

LOL, just how does a plant prepare to get munched on? hehehe... can you feel the plants pain... can you feel their PAIN MAN?

Urm, so you're not aware of plants that produce their own pesticides? They cannot move away (until we breed triffids!) but there is always something it can do that may aid its chances in survival. Again, you're asserting simplified facts just because reality seems a bit too bizarre or complex.

lol, it was just a HYPOTHETICAL example... to make a point, not a scientific study to prove anything... you can extrapolate those numbers and the number of rooms to any scale you like and the results will be the same... its probabilities and luck of the draw... your shortsightedness is YOUR weakness

Well again, you've completely missed the point. My point was that a simple division calculation is going to tell you precisely fuck all about what is going on with the data. I understand that it's hypothetical but the point still stands, just doing a sum and pointing at it to say that it's proof that sex determination happens your way is being rather forwards.

http://en.wikipedia.org/wiki/Normality_test
http://en.wikipedia.org/wiki/Analysis_of_variance

If you want to 'prove' something you need to at least first show if your data is normally distributed or not and then do some analytic tests to see which factors vary significantly (p>0.01 generally).

the effects you are seeing are do to changes in the epigenome either environmentally or chemically stressing the plant using epigenetic triggers... which doesn't effect the DNA of which X and Y chromosomes are a part of.

Environmental and chemical triggers are the same thing. I think you're still missing the idea. If the Y chromosome is not needed for the production of male-associated phenotypes then obviously the genes responsible may well not be located on the Y chromosome. If they aren't then this talk of X and Y gametes is moot in that regardless of whether a gamete contains the X or Y chromosome, the offspring retain the capability of producing pollen given the right conditions. These gametes cannot contain a Y chromosome yet further progeny are also capable of producing a male phenotype (i.e. pollen sacks) with an XX genotype given the correct stimuli/inhibition of hormone production.

but embryonic development had nothing to do with what I was saying.

I was under the impression that we were talking about environmental factors that could determine a plant's sex during from-seed development?

but the fact is after doing human genome studies we know that there are not enough genes in our DNA to account the variety of phenotypes... the differences between us are epigenetic... and epigenetic changes can be reversed by moving the chemical tags and turning the gene on or off

We have splice variants. Each gene can result in a host of differing mRNAs. Basically a gene is arranged in an exon a-intron-exon b-intron-exon c-intron-exon d. Introns are removed prior to the mRNA leaving the nucleus and the remaining exons can be rearranged so in this one gene we have the potential for 16 different proteins. And yes no doubt epigenetic changes are also involved in evolution but what changes? Again you're referring to an unbelievably massive area of biology as if it simply switches a gene on or off and that's it.

"mutate" you mean inherited... recombinant genetic pairing (in cannabis as in humans) results in "mutated" offspring... "mutated" meaning genetically different from either parent...

A mutation is a de-novo change in the genome mate. If you're going to assign the label mutant to an individual then we're all mutants - mutation occurs at a cellular level so it's cells that become mutated. Do you know what SNPs are? We have a huge amount of variability between individuals across the entire genome even within a species.

and if epigenetics doesn't allow for expression of latent ancestral traits then how do you explain the fact... that we share so much of our DNA with chimps but they resemble our primate ancestors so much more than we do... why is that?

are they expressing latent ancestral traits that have been suppressed in us Epigenetically?

See genetic splicing explanation given above. You also seem to be misunderstanding evolution slightly. A chimpanzee and all other animals/species on the planet are just as 'evolved' as the rest of us. Evolution is a divergence in genetics caused by mutations, not a ladder-style increase in evolvedness. My point was that these 'ancestral' traits have all been exposed to an additional x million years of random change in all species. Yes these genes/traits are held within humans, our cousins and our ancestors and are likely still expressed. As I said though, they have had millions of years of abuse from nature and are unlikely to exactly resemble anything found in earlier species, otherwise speciation wouldn't occur...

Epigenetics is dynamic and can undo and redo modifications to the structure, using the chemical tags can turn on or off expression...

Yes, in pluripotent cells and tumors...

those are all processes used in Epigenetic research that and PCR among others... I don't think Epigenetics is that vague; new sort of... relatively so, not well understood by many sure...

Well PCR flat out cannot show you any changes in epigenetics without further treatment to modify methylated bases with bisulfites. It's vague because the mechanisms I previously mentioned a) cannot be followed in vivo using current methods and b) occur very regularly without any impact on gene expression, CpG occurs extremely frequently throughout the genome yet only certain regions (CpG islands) can result in gene silencing? How?

ah ha, "completely unique in terms of it's MODIFIED structure"...

You're aware that DNA doesn't simply float around by itself in the nucleus? DNA is found as part of chromatin; when we take a closer look this appears to be DNA wrapped around protein spheres as in this image:



Now, protein chemistry and biochemistry in general is all about shapes and active sites. If the scaffold on which DNA is found is modified in structure, DNA becomes less or more available for transcription. This is the basis of why analyzing the genome of an organism doesn't tell you a whole lot about the organism itself.

Atavism

You're right. Provided a gene and all genes associated remain unchanged across millions of years and provided all regulatory systems break or fail to maintain a correct proteome then yes, certain characteristics that hark back to our evolutionary past can be observed, in the same manner that we can observe human embryos growing a coat of fur or rudimentary gills. It's not at all the same as saying that you can 'reverse evolve' a bird into a dinosaur, that's just not how it works. To give an example, the most common form of atavism in humans is having supernumary teeth. Slightly less exciting/extreme no? The point I was getting at is that the genetic material has changed to the extent that the organism represents a new species from its ancestor, they must be sufficiently genetically different from them to be incapable of producing fertile offspring so it would be slightly absurd to say that the only thing stopping us from turning into monkeys is a reversible modification of DNA.

Anyway, who's to say we are far from chimps?

I don't know how any of that pertains to the intersex traits observed in cannabis???

You keep blithely referring to epigenetics as if you know what it means. I was attempting to explain what it does actually mean.

maybe take your own advise ay?

I just graduated from a Biochemistry and Neuroscience degree and filed 30,000 words worth of dissertations on the role of epigenetics and de novo mutation in various diseases... As I keep saying, I don't mean to be an arse, just don't like seeing people asserting things that no one knows. If you were talking about 'Astral Weed' or 'God' I would be doing exactly the same

Riddle me this....

The main thing you realize in science is that there is no shame in admitting that you don't know Always be careful of people who say they know something for certain!

 

[Tonygreen]

Interesting paper...

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1691578/pdf/15058400.pdf

sex determination and the evolution of diocey from monoecy

 

[Infinitesimal]

Interesting paper...

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1691578/pdf/15058400.pdf

sex determination and the evolution of diocey from monoecy

[URL=https://www.icmag.com/ic/picture.php?albumid=42494&pictureid=1070306&thumb=5]View Image[/url]

that's it... and why DJ recommends using male herms that have sterile female flowers... except for why does it say the male is (YY) I wonder?

 

[DemonPigeon]

Infini, not definate on this, but I think the diagram is showing the ability to breed.

The "Male/Male" having sterile female flower (and eventually, perhaps, exclusively male flowers) compared to "Male/Female" hermie, so the plants in the diagram are just showing the Phenotype "xy" displays rather than a genotype of "yy".

Here's a fun diagram that may be better for cannabis

 

[Tonygreen]

More:

http://aob.oxfordjournals.org/content/86/2/211.full.pdf

"In Humulus species and its relative Cannabis, despite the
presence of X/autosome sex chromosome systems, sex
determination appears to be somewhat leaky"

 

[GMT]

Well I'm not too sure, if 'male' genes are present outside of the Y chromosome then it's rather pointless making that distinction as the difference would be entirely within the phenotypes and protein expression profiles of the plants. Saying that, the Y chromosome being a giant promoter/regulatory region is a wild guess so probably completely wrong Otherwise yeah, my bad, 3am posts are never the most thought out >.<

!

I think you're still associating genes that produce what are termed male flowers, with "maleness". I feel thats a mistake. Yes the genes responsible for generating male flowers are out side of the Y. That doesn't make it a pointless distinction though. A male isn't merely a phenotpe expression, its a genetic distinction. The primary difference being the inheritance. Far from being a wild guess, its the result of deductive logic and observational confirmation.
Most accept that feminized seeds can be created. If a male was merely a phenotype then that wouldn't be possible. If the genes for male flowers were not outside of the Y, then reversal wouldn't be possible. We see males that do not express female flowers, and if the Y didn't silence the production of female flowers, then that wouldn't be possible. Since we know the genes for producing male flowers, exist outside of the Y, then when we have 2 X's, we would also see male flowers on female plants without the X suppressing those genes or the male being needed to stimulate them. Therefore we can say with certainty, that in the absence of any chemical alteration (whether that be natural stresses or artificial external chemical additions) the X either stimulates the production of female flowers, the X silences the male flowers, the Y stimulates the male flowers and is stronger than the x's supression, or the Y silences the female flowers or some combination of the above. To say that describing the Y as a regulator is a mistake, I feel to be a mistake in itself. TO say that male is phenotype rather than genotype is a mistake also. A female only parentage gives rise to genetically female plants. A male female parentage generates male and female offspring. This is clearly genetic and not phenotype expression.

 

[DemonPigeon]

I'd categorize plants (ignoring mosaic plants and those carrying extra sex chromosomes) accordingly, probably everyone will disagree:

YX - "Genetic Male"
Male/Intersex Phenotyes possible depending on environment

XX - "Genetic Female"
Female/Intersex Phenotypes possible depending on environment

XY - "Genetic Intersex"
"Male" plants that carry other genes that make skew the phenotypic expression producing plants that are most likely intersex.

XX - "Genetic Intersex"
"Female" plants that carry other genes that make skew the phenotypic expression producing plants that are most likely intersex.

 

[GMT]

lol I'd simplify it, and just say good girls and boys and bad girls and boys.

 

[DemonPigeon]

And the bad ones grow plants?

edit: I was trying to imply you were refering to growers being "bad girls and boys"

 

[GMT]

if they didn't, how would we know if they were bad? an absence cannot be referred to as good or bad, merely absent.

 

[BullDogUK]

Since we know the genes for producing male flowers, exist outside of the Y, then when we have 2 X's, we would also see male flowers on female plants without the X suppressing those genes or the male being needed to stimulate them. Therefore we can say with certainty, that in the absence of any chemical alteration (whether that be natural stresses or artificial external chemical additions) the X either stimulates the production of female flowers, the X silences the male flowers, the Y stimulates the male flowers and is stronger than the x's supression, or the Y silences the female flowers or some combination of the above. To say that describing the Y as a regulator is a mistake, I feel to be a mistake in itself. TO say that male is phenotype rather than genotype is a mistake also. A female only parentage gives rise to genetically female plants. A male female parentage generates male and female offspring. This is clearly genetic and not phenotype expression.

This was a really great explanation GMT, cheers

To say that describing the Y as a regulator is a mistake, I feel to be a mistake in itself.

I have a feeling we may be misunderstanding each other slightly here so I'll try and break down the points again as it just makes it easier to get each point across without confusing things... Saying that I feel we're in agreement here? As I mentioned before I think it seems likely (to me! I'm a n00b at cannabis everyone) that, as we can force the expression of pollen sacs in female plants, that the genes responsible are located outside of the Y chromosome, leading to the conclusion that the Y chromosome may be involved in up-regulating the synthesis of 'male' proteins or the down-regulation of 'female' proteins, leading to:

TO say that male is phenotype rather than genotype is a mistake also.

Well, if we can force a female to produce pollen, does this not mean that the genes responsible for the sex phenotype are present in both males and females? In this case both 'males' and 'females' are technically both male and female in genotype.

I made a simplified diagram derived from the little summary you made (comic sans for extra humor):



So in this model, the X chromosome silences/down-regulates the production of 'male' proteins, resulting in the loss of pollen sacs and pollen production. The Y chromosome, on the other hand, up-regulates this synthesis, enough to overcome the down-regulation of the X chromosome. You also mention silencing of female flower production which I forgot to add in >.< but yes, that also makes sense.

Either way, we know that females are capable of producing pollen sacs. Regardless of whether the pollen contains X or Y chromosomes, this will still lead to the production of fertile offspring, capable of a repeated 'maleized' female x female crossings correct? If this is the case, then this is what I mean by the distinction being somewhat irrelephant. Obviously in nature this isn't going to be a successful survival mechanism (thus why we see Y chromosome males I guess?).

 

[GMT]

Well, if we can force a female to produce pollen, does this not mean that the genes responsible for the sex phenotype are present in both males and females?

yes

In this case both 'males' and 'females' are technically both male and female in genotype.

no. a female does not silence the production of female flowers, a male does not silence the production of pollen, a pretty important distinction for both growers of buds and breeders of seeds.

Either way, we know that females are capable of producing pollen sacs. Regardless of whether the pollen contains X or Y chromosomes, this will still lead to the production of fertile offspring,

yes

capable of a repeated 'maleized' female x female crossings correct?

lol maleized, technically if you are using that term in the way we use feminized, then no as maleized would only produce male seeds and what you are describing can only ever produce female seeds.

If this is the case, then this is what I mean by the distinction being somewhat irrelephant. Obviously in nature this isn't going to be a successful survival mechanism (thus why we see Y chromosome males I guess?).

if one can breed and one cannot without the use of chemicals, if one fills half your room with males and the other fills all your room with females, if one is genetically different from the other, how can that be considered irrelevant?

Not trying to bust your balls mate, just this is pretty important to understand.

 

[BullDogUK]

lol maleized, technically if you are using that term in the way we use feminized, then no as maleized would only produce male seeds and what you are describing can only ever produce female seeds.

Still think we're misunderstand here by maleized I mean a female that's been forced to produce pollen. Obviously all the pollen it produces will contain only X.

no. a female does not silence the production of female flowers, a male does not silence the production of pollen, a pretty important distinction for both growers of buds and breeders of seeds.

Not quite sure I understand you here... So yes, a female does not silence the production of female flowers, leading to flower production. Nor do males silence the production of pollen, leading to pollen production. My point is that regardless of whether a plant is male or female, given the correct stimuli, pollen can be produced. Now my understanding is that in plant sexual reproduction we refer to the pollen producer as 'male' and the pollen receiver/female flower producer as 'female'. The point being that females would be unable to express pollen sacks if they were not also of a 'male' genotype as these pollen sacks are not being pulled out of thin air, the plants must already contain the required genes. It may well be that we have differing definitions of male and female here but evidently the plants do not require a Y chromosome to produce the male sex organ.

if one can breed and one cannot without the use of chemicals, if one fills half your room with males and the other fills all your room with females, if one is genetically different from the other, how can that be considered irrelevant?

Well it's not irrelevant and we're talking hypothetically here so I didn't see a problem with being able to force as many plants into producing pollen sacks as you wish without any problems with the health of the plant. Like I said, that's not the case in nature thus why we don't see it too much in wild plants (I'd assume?).

But once again, the males and females obviously contain a different genome but this is irrelevant due to the ability of females to form the male sex organ, leading to the conclusion that the plant's ability to act as a male in the reproductive process is not reliant on the presence of the Y chromosome/the differing genotypes.

In terms of breeding - surely it is possible to take the progeny of females x 'converted' (less confusing name haha) females and introduce them into standard female x male crosses? The only downshot being that the female x c female progeny will all be female.

 

[DemonPigeon]

It's interesting to note that "male" hermaphrodites do exist but due to males usually dieing after pollen release concludes these are highly unlikely to reproduce.

Ultimately seed production is (on an individual level) an inferior survival strategy to pollen production, a large male may have millions of potential offspring, a huge female mere thousands.
Hemaphroditism signifficantly raises the odds for those pistilate plants in many scenarios, in the wild, in traditional farms, even modern grow rooms.

 

[Tonygreen]

Is it possible cannabis is in the middle of evolving dioecy from monoecy and is not finished the process yet?

 

[GMT]

well the thing is bulldog, we aren't all mad scientists with potions bubbling and jars filled with newt eyes or bat hearts on the shelves Some of us are simple minded canna farmers. So why would we want to force something to happen unnaturally when we can sit back and let it happen naturally. There is also the well worn argument about working the male line along side the female line of a strain. Yes we can FORCE pollen out of the female plant. Yes its perfectly good pollen that wont hurt the offspring. Yes there are arguments to be made in favour of doing that even. And yes I wish the spell checker wasn't american here telling me there's no U in favour lol. But the fact that we have to force the females to do this, tells us they are absolutely different from males. Not just in expression, but in content. And so, what we have been discussing ie are males just phenotypically different from females, is pretty clear in my mind. Therefore to refer to a female that produces pollen as the father or a male is inaccurate. And to say that a female contains a male genotype is inaccurate. It contains the instruction sets (genes) to produce pollen sacks, but that's not saying the same thing.


Tony, kinda strain dependent, also well worked v landrace dependent in some cases, or pollen chucker v breeder dependent, but yes in a lot of cases I'd agree with that.