Surely we can see that the autosonal regions are also responsible for the addadicktome triggers.
Heritability of Intersex Traits
- Thread starter Tom Hill
- Start date
is it that bad
?,,,, thanks for thinking about it ither way Green
im finding it had to get a copy of that paper your referencing for free ,,,,,ive only read the abstract,,but couldnt the recombination of [PAR] be part of a more complex transpoon type activity?,,,,,,as far as i can tell there is only indirect evidence of an Active Y,,not direct evidence,,,,,please correct me if im wrong..
but i am quoting from papers after [2005] now,,,,,,,,,,,
[E Kejnovsky, R Hobza, T Cermak, Z Kubat and B Vyskot. 2009]
The trajectory from autosomes to sex chromosomes may start with the emergence of a sex-determining gene with one allele that determines male individuals and the other female individuals. A two-loci model was suggested by Charlesworth et al. (2005) in which mutation in one gene on the proto-X chromosome results in male sterility and mutation in another gene on the proto-Y chromosome results in female sterility. Acquisition of a sex-determining gene(s) may be followed by the suppression of recombination in the vicinity of the gene(s). Later, other sex-determining genes that influence the development of a particular sex, or are antagonistic to the opposing sex, may accumulate around the sexdetermining gene. Such sex-determining regions can, in some instances, translocate between chromosomes and create new sex chromosomes (Traut and Willhoeft, 1990; Willhoeft and Traut, 1990; Traut and Wollert, 1998). The initiating mechanisms of recombination suppression are not yet clear, though some models based on epigenetic silencing (Jablonka, 2004) or inversions (Lahn and Page,1999) have been proposed. Zluvova et al. (2005) suggested that the inversion on the Y chromosome of Silene latifolia is a consequence of recombination arrest as opposed to its cause. In addition, non-recombining regions may expand through the accumulation of repetitive DNA sequences (Charlesworth, 1991), which often form heterochromatin. Ultimately the processes, because of a lack of recombination in meiosis, may lead to a lower expression of the Y-linked genes and eventually to their degeneration into pseudogenes (Bachtrog, 2006; Marais et al., 2008). Once the Y chromosome has become a genetic desert, the balance between mechanisms that expand the chromosome (for example, transposition) and those that cause it to contract (for example, deletions), will govern the longterm fate of the chromosome. At this stage, large regions of the Y chromosome without genes are dispensable and can be lost. It is not clear yet whether the processes of gene degeneration, TEs accumulation and expansions on one hand and contractions on the other hand are stepwise or are occurring simultaneously. However, the lifetime of an old Y chromosome is often prolonged by the addition of segments transferred from autosomes (Graves, 2005). Acquisition of new genes from autosomes mediated by retrotransposition has been shown in humans (Lahn and Page, 1999), and a similar duplicative transfer has also been shown in the young Y chromosomes of Silene latifolia (Matsunaga et al., 2003). A final possibility is that sex is determined not by the specific Y-linked gene, but only by the ratio of X chromosome to autosomes (X/A ratio). Then the Y chromosome either remains as a genetic entity or could be lost entirely. A new autosomal pair can then be chosen to become a new pair of sex chromosomes and the cyclic process can continue. The persistence of the Y chromosome indicates that it can repeatedly arise de novo, for example, by the fusion between an autosome and an X chromosome followed by the fixation of the neo-X and the neo-Y chromosomes as was shown in grasshopper Podisma pedestris (Westerman and Hewitt, 1985; Veltsos et al., 2008)
http://www.evolucnigenomika.cz/pdf/Kejnovsky_09_Heredity.pdf
?,,,, thanks for thinking about it ither way Greenim finding it had to get a copy of that paper your referencing for free ,,,,,ive only read the abstract,,but couldnt the recombination of [PAR] be part of a more complex transpoon type activity?,,,,,,as far as i can tell there is only indirect evidence of an Active Y,,not direct evidence,,,,,please correct me if im wrong..
but i am quoting from papers after [2005] now,,,,,,,,,,,
[E Kejnovsky, R Hobza, T Cermak, Z Kubat and B Vyskot. 2009]
The trajectory from autosomes to sex chromosomes may start with the emergence of a sex-determining gene with one allele that determines male individuals and the other female individuals. A two-loci model was suggested by Charlesworth et al. (2005) in which mutation in one gene on the proto-X chromosome results in male sterility and mutation in another gene on the proto-Y chromosome results in female sterility. Acquisition of a sex-determining gene(s) may be followed by the suppression of recombination in the vicinity of the gene(s). Later, other sex-determining genes that influence the development of a particular sex, or are antagonistic to the opposing sex, may accumulate around the sexdetermining gene. Such sex-determining regions can, in some instances, translocate between chromosomes and create new sex chromosomes (Traut and Willhoeft, 1990; Willhoeft and Traut, 1990; Traut and Wollert, 1998). The initiating mechanisms of recombination suppression are not yet clear, though some models based on epigenetic silencing (Jablonka, 2004) or inversions (Lahn and Page,1999) have been proposed. Zluvova et al. (2005) suggested that the inversion on the Y chromosome of Silene latifolia is a consequence of recombination arrest as opposed to its cause. In addition, non-recombining regions may expand through the accumulation of repetitive DNA sequences (Charlesworth, 1991), which often form heterochromatin. Ultimately the processes, because of a lack of recombination in meiosis, may lead to a lower expression of the Y-linked genes and eventually to their degeneration into pseudogenes (Bachtrog, 2006; Marais et al., 2008). Once the Y chromosome has become a genetic desert, the balance between mechanisms that expand the chromosome (for example, transposition) and those that cause it to contract (for example, deletions), will govern the longterm fate of the chromosome. At this stage, large regions of the Y chromosome without genes are dispensable and can be lost. It is not clear yet whether the processes of gene degeneration, TEs accumulation and expansions on one hand and contractions on the other hand are stepwise or are occurring simultaneously. However, the lifetime of an old Y chromosome is often prolonged by the addition of segments transferred from autosomes (Graves, 2005). Acquisition of new genes from autosomes mediated by retrotransposition has been shown in humans (Lahn and Page, 1999), and a similar duplicative transfer has also been shown in the young Y chromosomes of Silene latifolia (Matsunaga et al., 2003). A final possibility is that sex is determined not by the specific Y-linked gene, but only by the ratio of X chromosome to autosomes (X/A ratio). Then the Y chromosome either remains as a genetic entity or could be lost entirely. A new autosomal pair can then be chosen to become a new pair of sex chromosomes and the cyclic process can continue. The persistence of the Y chromosome indicates that it can repeatedly arise de novo, for example, by the fusion between an autosome and an X chromosome followed by the fixation of the neo-X and the neo-Y chromosomes as was shown in grasshopper Podisma pedestris (Westerman and Hewitt, 1985; Veltsos et al., 2008)
http://www.evolucnigenomika.cz/pdf/Kejnovsky_09_Heredity.pdf
The active male linked Y that is responsible for the production of a plant's maleness may just be coding for a certain type or types of hormones/proteins that activate the part of the genome that contains the physical architecture of maleness. The sex reversal treatments likely mimic this natural system.
In other words: the sex determinism genes aren't the sex differentiation genes.
is it that bad
im finding it had to get a copy of that paper your referencing for free ,,,,,ive only read the abstract,,but couldnt the recombination of [PAR] be part of a more complex transpoon type activity?,,,,,,as far as i can tell there is only indirect evidence of an Active Y,,not direct evidence,,,,,please correct me if im wrong..
Couldn't it be a more complex transpoon type activity? What are you even bloody talking about dude. Parts of the Y recombine with the X. DEAL WITH IT. Is it hard to believe that now because you've set up some horrible 5 point system that you must follow pointlessly aaahhhhhhh dogma's great.
Only indirect evidence of an active Y? WHAAAAAAT? Why do you think they call it a Y chromosome and not just chromosome A? They've found male specific markers on the Y chromosome. Game over.
Ugh, do you not see all the speculation in that piece. How many more times could they say 'may.' They're trying to understand how all these mechanisms arise. How is this helpful with respect to cannabis. Frankly why does it even matter if it's an X/autosome or XY system? Regardless, we would be breeding/treating the plants the same. And you have listed NO EVIDENCE for an X/autosome system. Please feel free to list some since you seem to think we only see indirect evidence of an active Y system.
Rick I honestly thought I had laid out my position as clearly as was possible using the english language. but just to put it in the simplest language, no I dont believe in an active Y that does anything other than silence the X or an active X that does anything other than silence the Y. I think right now if what is posted isnt understood theres little point in posting it. Its fine to google and cut and copy stuff, but if you and green dont actually read it and just want to slate each others google finds, theres little point in copy and pasting them. It would be nice if I thought either of you understood half of what you were pasting, but each time you both then ask the other some pointless stupid question that is clearly already answered if the poece was even read. I've had enough now. Have a copy and paste war because neither of you are interested in understanding, just copying something to defend.
Feel free to explain to me anything you think I don't understand.
GMT,,,,that last post just seems to be lot clearer than all your other posts,,,you can oviously formulate a better argument than i can for an X/autosome dossage system,,,,please do bro,,please do,,,,from your last post it looks like you believe in the X/autosome system from Ainsworth??,,,,,what you just posted is exactly how i understand things,,,,the Y is a silencer but you seem to be on the X/Autosome team?
Green..
i just thought [maybe] the recombination thats happening in the PAR might be because of aquisition of genes from the autosome,,,so the Y would still degrading,,,,but its not the best argument....
i dont dissagree with you Green,,,,but im sure your about to tell me the Y is not dispencable,,,,are you bro?,,,,didnt sam say it was novel?
sorry for the copy and paste
[E Kejnovsky, R Hobza, T Cermak, Z Kubat and B Vyskot. 2009]
"the lifetime of an old Y chromosome is often prolonged by the addition of segments transferred from autosomes (Graves, 2005). Acquisition of new genes from autosomes mediated by retrotransposition has been shown in humans (Lahn and Page, 1999), and a similar duplicative transfer has also been shown in the young Y chromosomes of Silene latifolia (Matsunaga et al., 2003)."
Green
..i just thought [maybe] the recombination thats happening in the PAR might be because of aquisition of genes from the autosome,,,so the Y would still degrading,,,,but its not the best argument....
i dont dissagree with you Green,,,,but im sure your about to tell me the Y is not dispencable,,,,are you bro?,,,,didnt sam say it was novel?
sorry for the copy and paste
[E Kejnovsky, R Hobza, T Cermak, Z Kubat and B Vyskot. 2009]
"the lifetime of an old Y chromosome is often prolonged by the addition of segments transferred from autosomes (Graves, 2005). Acquisition of new genes from autosomes mediated by retrotransposition has been shown in humans (Lahn and Page, 1999), and a similar duplicative transfer has also been shown in the young Y chromosomes of Silene latifolia (Matsunaga et al., 2003)."
Stop posting pointless speculation about the evolutionary processes that may or may not have occurred in other species' Y. It has dick all to do with cannabis and obviously you're grasping at straws. GMT is right, you often don't even know what you're linking.
fair enough,,,if you think its that bad,,il stop
it was nice to hear your view on it,,,,thanks
it was nice to hear your view on it,,,,thanks
Thanks.
Just noticed hyb got banned again Lets keep running around in circles folks.
Just noticed hyb got banned again
Lets keep running around in circles folks.
seiously,,,i apreceate your imput with me Green,,,you doing me a favour,,,you and me both know im just a newbi whos dreaming,,,,seirously thankyou,,,,
thats some bad news again with hyb,,,,im pissed kopite aint here to say something too,,,its daft this banning thing,,,,i was waiting for his imput here,,,im allways gutted when he gets let go,,,i believe we ow him more than that,,,
thats some bad news again with hyb,,,,im pissed kopite aint here to say something too,,,its daft this banning thing,,,,i was waiting for his imput here,,,im allways gutted when he gets let go,,,i believe we ow him more than that,,,
I do miss kopite.
hyb is sure to be around
Liking the thread guys!
hyb is sure to be around
Liking the thread guys!
This gets close to my position with one alteration needed.
Rather than an active X/Y I see an opressive X/Y system. The X produces proteins that switch off the pollen coding etc, and the Y produces both protiens to switch off both the production of pistils, and also the production of those proteins which prevent the production of pollen etc. Thereby allowing the male part of the genome to be active without the X part silencing it. In that system its also easy to imagine why the Y is larger in such a system.
The key is what happens when we add a chemical inhibitor.
Oh and Rick, a sterile male in this system would be caused by either a fault in the gene that makes pollen or a fault in the Y that prevents the protiens being made by the X which turn off the pollen production.
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now this is getting good
that was pretty clear post,,,
so, whats the deal with fem seeds expressing maleness,,,?
remember my mirical SSH[f] x OGKA[f] male,,,it fliped into a female monster yealder,,with super vigor
that was pretty clear post,,,
so, whats the deal with fem seeds expressing maleness,,,?
remember my mirical SSH[f] x OGKA[f] male,,,it fliped into a female monster yealder,,with super vigor
what do you think about Ainsworths saying Cannabis is using an X/Autosome dosage system?...
The only thing Ainsworth says in the paper you listed is that cannabis is an X/autosome system. You need to find the paper he referenced when he made that assertion to get any facts on it.
GMT- It's my understanding that even if the X and Y work as opposite inhibitors it would still be classified as an active Y system. Because if you have the Y chromosome then you're male.
Also can you further your idea why the Y would be larger in this case. Not really following you on that point.
And if you could explain to me anything you thought I got wrong in here I'd be thankful.
GMT- It's my understanding that even if the X and Y work as opposite inhibitors it would still be classified as an active Y system. Because if you have the Y chromosome then you're male.
Also can you further your idea why the Y would be larger in this case. Not really following you on that point.
And if you could explain to me anything you thought I got wrong in here I'd be thankful.
im trying to find [Yamada 1943],,,,,,,anyone heard of this dude beffore?
[from Ainsworth 2000]....
http://aob.oxfordjournals.org/cgi/reprint/86/2/211.pdf
"Di€erentiated sex chromosomes have been established clearly in only six families, representing about eight species and two major species groups. In the Cannabidaceae, which comprises three species only, Humulus lupulus (the culti-vated hop), H. japonicus and Cannabis sativa, all are dioecious and have evolved sex chromosomes of the X/autosome dosage type (Jacobsen, 1957; Parker, 1990)."
im also finding it hard to find (Jacobsen, 1957; Parker, 1990),,,,
[from Ainsworth 2000]....
http://aob.oxfordjournals.org/cgi/reprint/86/2/211.pdf
"Di€erentiated sex chromosomes have been established clearly in only six families, representing about eight species and two major species groups. In the Cannabidaceae, which comprises three species only, Humulus lupulus (the culti-vated hop), H. japonicus and Cannabis sativa, all are dioecious and have evolved sex chromosomes of the X/autosome dosage type (Jacobsen, 1957; Parker, 1990)."
im also finding it hard to find (Jacobsen, 1957; Parker, 1990),,,,
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It's a double reference so you'll have to dig up this one too:
Parker JS. 1990. Sex chromosomes and sexual differentiation in Flowering plants. Chromosomes Today 10: 187±198
Regardless Ainsworth is going off some old information when making the judgment that cannabis is X/a type. But he does reference the 1995 male marker study in cannabis so he's at least aware of it.
Parker JS. 1990. Sex chromosomes and sexual differentiation in Flowering plants. Chromosomes Today 10: 187±198
Regardless Ainsworth is going off some old information when making the judgment that cannabis is X/a type. But he does reference the 1995 male marker study in cannabis so he's at least aware of it.
