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its all down to genetics
#1
So, branching a bit from my usual research, this particular thread is dedicated to specifics about genetics. in it, I will post findings and research only about biological and genetic findings. the who's how's and why's.

differentiation of the female and male anatomy will also be discussed.


perhaps with the posted information , one of us can figure out for certainty, how to switch (if possible) the triggers and mechanisms in our bodies from male to female.



I strongly encourage, anyone reading this thread, to not only read the entire articles on the hyperlinks, but also click on the embedded hyperlinks within the articles, for a better understanding of what is being talked about.

To be informed, is to make better decisions.
your body is like Lego's, with the right building blocks and imagination you can build anything!
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#2
Duct, duct , goose!

AMH gene- can we turn it off? and reverse nature?


The AMH GENE, is expressed during fetal development:

https://en.wikipedia.org/wiki/Anti-M%C3%...an_hormone

Anti-Müllerian hormone (AMH), also known by various other names, is a protein that in humans is encoded by the AMH gene.[1] It is a hormone that inhibits the development of the Müllerian ducts (paramesonephric ducts) in the male embryo.[2]
Although the AMH receptor is expressed in both male and female fetuses, AMH expression has been isolated to male sertoli cells.[3] Expression of AMH is activated by SOX9 in the male Sertoli cells and causes the irreversible regression of the Müllerian ducts.[4] Because AMH expression is critical to sex differentiation at a specific time during fetal development, it appears to be tightly regulated by SF1, GATA factors, DAX1 and FSH.[5][6][7] Mutations in both the AMH gene and the type II AMH receptor have been shown to cause the persistence of Müllerian derivatives in males that are otherwise normally virilized.[8]
AMH expression also occurs in ovarian granulosa cells of females postpartum, and serves as a molecular biomarker for relative size of the ovarian reserve.[9] In humans, the number of cells in the follicular reserve can be used to predict timing of menopause.[10] In bovine, AMH can be used for selection of females in multi-ovulatory embryo transfer programs by predicting the number of antral follicles developed to ovulation.[11]




https://ghr.nlm.nih.gov/gene/AMH

The AMH gene provides instructions for making a protein that is involved in male sex differentiation. During development of male fetuses, the AMH protein is produced and released (secreted) by cells of the testes. The secreted protein attaches (binds) to its receptor, which is found on the surface of Müllerian duct cells. The Müllerian duct, found in both male and female fetuses, is the precursor to the female reproductive organs. Binding of the AMH protein to its receptor induces self-destruction (apoptosis) of the Müllerian duct cells. As a result, the Müllerian duct breaks down (regresses) in males. In females, who do not produce the AMH protein during fetal development, the Müllerian duct becomes the uterus and fallopian tubes.

https://en.wikipedia.org/wiki/Paramesonephric_duct (mullerian ducts, part of the female reproductive system).
Paramesonephric ducts (or Müllerian ducts) are paired ducts of the embryo that run down the lateral sides of the urogenital ridge and terminate at the sinus tubercle in the primitive urogenital sinus. In the female, they will develop to form the uterine tubes, uterus, cervix, and the upper one-third of the vagina;[1] in the male, they are lost. These ducts are made of tissue of mesodermal origin.[2]
Embryogenesis[edit]

In mammals, AMH prevents the development of the Müllerian ducts into the uterus and other Müllerian structures.[2] The effect is ipsilateral, that is each testis suppresses Müllerian development only on its own side.[14] In humans, this action takes place during the first 8 weeks of gestation. If no hormone is produced from the gonads, the Müllerian ducts automatically develop, while the Wolffian ducts, which are responsible for male reproductive parts, automatically die.[15] Amounts of AMH that are measurable in the blood vary by age and sex. AMH works by interacting with specific receptors on the surfaces of the cells of target tissues (anti-Müllerian hormone receptors). The best-known and most specific effect, mediated through the AMH type II receptors, includes programmed cell death (apoptosis) of the target tissue (the fetal Müllerian ducts).


the question that comes to mind is, can one de-activate the amh gene, and cause the body to convert the testes into ovaries? in some cases, there are people with ovo-testes.. part ovaries, part testies, either one or both of the testes can be ovotestes. in some cases, people have one testes, one ovary.. (see intersexed conditions). Though it is plainly states that once the protein is bound to the receptor, the mullerian ducts go away and the wolffian ducts are produced, is there a possible way to swtich them from wolfian ducts to mullerian ducts? 

More research to follow.
your body is like Lego's, with the right building blocks and imagination you can build anything!
 Reply
#3
hmm , interesting :
https://en.wikipedia.org/wiki/Paramesonephric_duct

Mutations in AMH[edit]

Individuals that are 46, XY and have been tested positive for mutations in their AMH or AMH receptor genes have been known to exhibit features typical of that which are exhibited in persistent müllerian duct syndrome due to the fact that the paramesonephric ducts fail to regress. When this happens the individuals develop structures that are derived from the paramesonephric duct, and also structures that are derived from the mesonephric duct. A male that has persistent müllerian duct syndrome may have an upper vagina, uterus, and uterine tubes as well as ductus deferens along with male external genitalia. The female organs are in the correct anatomical position but the position of the testis varies. 60% to 70% of detected cases, both testes will lie in the normal position for the ovaries; about 20% to 30% of the time, one of the testis will lie within the inguinal hernial sac while in other cases both testes will lie within the same inguinal hernia sac. However whenever an individual exhibits persistent müllerian duct syndrome, the ductus deferens will run along the lateral sides of the uterus.[8]

so this leads to the possibility of a "male" being not so male, other than appearance. as the article states, a test would be needed for a mutation of the amh gene or its receptor.
your body is like Lego's, with the right building blocks and imagination you can build anything!
 Reply
#4
something to turn the gene expressions on/off:

S-adenosylmethionine synthetase enzyme:
https://en.wikipedia.org/wiki/S-adenosyl...ase_enzyme

AdoMet is a methyl donor for transmethylation. It gives away its methyl group and is also the propylamino donor in polyamine biosynthesis. S-adenosylmethionine synthetase can be considered the rate-limiting step of the methionine cycle.[2]
S-adenosylmethionine (SAM) is a methyl donor and allows DNA methylation. Once DNA is methylated, it switches the genes off and therefore, S-adenosylmethionine can be considered to control gene expression.[3]
SAM is also involved in gene transcription, cell proliferation, and production of secondary metabolites.[4] Hence SAM synthetase is fast becoming a drug target, in particular for the following diseases: depression, dementia, vacuolar myelopathy, liver injury, migraine, osteoarthritis, and as a potential cancer chemopreventive agent.[5]

Found on AMAZON.com :
https://www.amazon.com/Pure-Encapsulatio...ransferase 
Pure Encapsulations - SAMe (S-Adenosylmethionine) - Hypoallergenic Supplement to Support Positive Mood and Cognitive Function* $60/bottle

more research to follow .
your body is like Lego's, with the right building blocks and imagination you can build anything!
 Reply
#5
(05-10-2016, 10:51 PM)Tanya Marie Squirrel Wrote: Duct, duct , goose!

AMH gene- can we turn it off? and reverse nature?


The AMH GENE, is expressed during fetal development:

https://en.wikipedia.org/wiki/Anti-M%C3%...an_hormone

Anti-Müllerian hormone (AMH), also known by various other names, is a protein that in humans is encoded by the AMH gene.[1] It is a hormone that inhibits the development of the Müllerian ducts (paramesonephric ducts) in the male embryo.[2]
Although the AMH receptor is expressed in both male and female fetuses, AMH expression has been isolated to male sertoli cells.[3] Expression of AMH is activated by SOX9 in the male Sertoli cells and causes the irreversible regression of the Müllerian ducts.[4] Because AMH expression is critical to sex differentiation at a specific time during fetal development, it appears to be tightly regulated by SF1, GATA factors, DAX1 and FSH.[5][6][7] Mutations in both the AMH gene and the type II AMH receptor have been shown to cause the persistence of Müllerian derivatives in males that are otherwise normally virilized.[8]
AMH expression also occurs in ovarian granulosa cells of females postpartum, and serves as a molecular biomarker for relative size of the ovarian reserve.[9] In humans, the number of cells in the follicular reserve can be used to predict timing of menopause.[10] In bovine, AMH can be used for selection of females in multi-ovulatory embryo transfer programs by predicting the number of antral follicles developed to ovulation.[11]




https://ghr.nlm.nih.gov/gene/AMH

The AMH gene provides instructions for making a protein that is involved in male sex differentiation. During development of male fetuses, the AMH protein is produced and released (secreted) by cells of the testes. The secreted protein attaches (binds) to its receptor, which is found on the surface of Müllerian duct cells. The Müllerian duct, found in both male and female fetuses, is the precursor to the female reproductive organs. Binding of the AMH protein to its receptor induces self-destruction (apoptosis) of the Müllerian duct cells. As a result, the Müllerian duct breaks down (regresses) in males. In females, who do not produce the AMH protein during fetal development, the Müllerian duct becomes the uterus and fallopian tubes.

https://en.wikipedia.org/wiki/Paramesonephric_duct (mullerian ducts, part of the female reproductive system).
Paramesonephric ducts (or Müllerian ducts) are paired ducts of the embryo that run down the lateral sides of the urogenital ridge and terminate at the sinus tubercle in the primitive urogenital sinus. In the female, they will develop to form the uterine tubes, uterus, cervix, and the upper one-third of the vagina;[1] in the male, they are lost. These ducts are made of tissue of mesodermal origin.[2]
Embryogenesis[edit]

In mammals, AMH prevents the development of the Müllerian ducts into the uterus and other Müllerian structures.[2] The effect is ipsilateral, that is each testis suppresses Müllerian development only on its own side.[14] In humans, this action takes place during the first 8 weeks of gestation. If no hormone is produced from the gonads, the Müllerian ducts automatically develop, while the Wolffian ducts, which are responsible for male reproductive parts, automatically die.[15] Amounts of AMH that are measurable in the blood vary by age and sex. AMH works by interacting with specific receptors on the surfaces of the cells of target tissues (anti-Müllerian hormone receptors). The best-known and most specific effect, mediated through the AMH type II receptors, includes programmed cell death (apoptosis) of the target tissue (the fetal Müllerian ducts).


the question that comes to mind is, can one de-activate the amh gene, and cause the body to convert the testes into ovaries? in some cases, there are people with ovo-testes.. part ovaries, part testies, either one or both of the testes can be ovotestes. in some cases, people have one testes, one ovary.. (see intersexed conditions). Though it is plainly states that once the protein is bound to the receptor, the mullerian ducts go away and the wolffian ducts are produced, is there a possible way to swtich them from wolfian ducts to mullerian ducts? 

More research to follow.


Some thoughts on turning off the amh gene:

From above: "Expression of AMH is activated by SOX9" If you turn off SOX9 would it not deactivate the AMH?

See Figure 3 from this article - http://onlinelibrary.wiley.com/doi/10.10...900193/pdf 

According to this article the FOXL2 gene suppresses the SOX9 gene. From some reading I did in the past, FOXL2 is found in the ovaries of all mammalian vertebrate species so by my thinking, this should be found in cow ovaries. So if one were to smear some sort of Bovine Ovary cream on their boys... Oh wait, that's what I've been doing for the past few weeks. I'm not sure whether that would be enough to flip that testes to ovary switch, but I might just find out.

I don't think you would be able to switch ducts though, seems to me the Müllerian duct is destroyed by AMH is it not?

Anyway, interesting articles, thanks for posting.
 Reply
#6
(07-10-2016, 08:10 AM)Grew_Some Wrote:
(05-10-2016, 10:51 PM)Tanya Marie Squirrel Wrote: Duct, duct , goose!

AMH gene- can we turn it off? and reverse nature?


The AMH GENE, is expressed during fetal development:

https://en.wikipedia.org/wiki/Anti-M%C3%...an_hormone

Anti-Müllerian hormone (AMH), also known by various other names, is a protein that in humans is encoded by the AMH gene.[1] It is a hormone that inhibits the development of the Müllerian ducts (paramesonephric ducts) in the male embryo.[2]
Although the AMH receptor is expressed in both male and female fetuses, AMH expression has been isolated to male sertoli cells.[3] Expression of AMH is activated by SOX9 in the male Sertoli cells and causes the irreversible regression of the Müllerian ducts.[4] Because AMH expression is critical to sex differentiation at a specific time during fetal development, it appears to be tightly regulated by SF1, GATA factors, DAX1 and FSH.[5][6][7] Mutations in both the AMH gene and the type II AMH receptor have been shown to cause the persistence of Müllerian derivatives in males that are otherwise normally virilized.[8]
AMH expression also occurs in ovarian granulosa cells of females postpartum, and serves as a molecular biomarker for relative size of the ovarian reserve.[9] In humans, the number of cells in the follicular reserve can be used to predict timing of menopause.[10] In bovine, AMH can be used for selection of females in multi-ovulatory embryo transfer programs by predicting the number of antral follicles developed to ovulation.[11]




https://ghr.nlm.nih.gov/gene/AMH

The AMH gene provides instructions for making a protein that is involved in male sex differentiation. During development of male fetuses, the AMH protein is produced and released (secreted) by cells of the testes. The secreted protein attaches (binds) to its receptor, which is found on the surface of Müllerian duct cells. The Müllerian duct, found in both male and female fetuses, is the precursor to the female reproductive organs. Binding of the AMH protein to its receptor induces self-destruction (apoptosis) of the Müllerian duct cells. As a result, the Müllerian duct breaks down (regresses) in males. In females, who do not produce the AMH protein during fetal development, the Müllerian duct becomes the uterus and fallopian tubes.

https://en.wikipedia.org/wiki/Paramesonephric_duct (mullerian ducts, part of the female reproductive system).
Paramesonephric ducts (or Müllerian ducts) are paired ducts of the embryo that run down the lateral sides of the urogenital ridge and terminate at the sinus tubercle in the primitive urogenital sinus. In the female, they will develop to form the uterine tubes, uterus, cervix, and the upper one-third of the vagina;[1] in the male, they are lost. These ducts are made of tissue of mesodermal origin.[2]
Embryogenesis[edit]

In mammals, AMH prevents the development of the Müllerian ducts into the uterus and other Müllerian structures.[2] The effect is ipsilateral, that is each testis suppresses Müllerian development only on its own side.[14] In humans, this action takes place during the first 8 weeks of gestation. If no hormone is produced from the gonads, the Müllerian ducts automatically develop, while the Wolffian ducts, which are responsible for male reproductive parts, automatically die.[15] Amounts of AMH that are measurable in the blood vary by age and sex. AMH works by interacting with specific receptors on the surfaces of the cells of target tissues (anti-Müllerian hormone receptors). The best-known and most specific effect, mediated through the AMH type II receptors, includes programmed cell death (apoptosis) of the target tissue (the fetal Müllerian ducts).


the question that comes to mind is, can one de-activate the amh gene, and cause the body to convert the testes into ovaries? in some cases, there are people with ovo-testes.. part ovaries, part testies, either one or both of the testes can be ovotestes. in some cases, people have one testes, one ovary.. (see intersexed conditions). Though it is plainly states that once the protein is bound to the receptor, the mullerian ducts go away and the wolffian ducts are produced, is there a possible way to swtich them from wolfian ducts to mullerian ducts? 

More research to follow.


Some thoughts on turning off the amh gene:

From above: "Expression of AMH is activated by SOX9" If you turn off SOX9 would it not deactivate the AMH?

See Figure 3 from this article - http://onlinelibrary.wiley.com/doi/10.10...900193/pdf 

According to this article the FOXL2 gene suppresses the SOX9 gene. From some reading I did in the past, FOXL2 is found in the ovaries of all mammalian vertebrate species so by my thinking, this should be found in cow ovaries. So if one were to smear some sort of Bovine Ovary cream on their boys... Oh wait, that's what I've been doing for the past few weeks. I'm not sure whether that would be enough to flip that testes to ovary switch, but I might just find out.

I don't think you would be able to switch ducts though, seems to me the Müllerian duct is destroyed by AMH is it not?

Anyway, interesting articles, thanks for posting.


I did read a piece a few years ago where they where looking into tho posibility of being able to use gene's to flip the testes.
Sex, its what's on your drivers license.
Gender, its how you feel inside.

DUFF - Designated Unique Feminine Friend.
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#7
thanks both, for the addition to this thread! interesting to know. Jannet, can you dredge up that info? I would be interested to read it as well.

grewsome:: , thanks I will look into and read that link. appreciated.

lol let me know how your scientific study works on your transdermal application Smile

sounds similar to my bov thread about site-specific application (in my case, the breast area).
your body is like Lego's, with the right building blocks and imagination you can build anything!
 Reply
#8
so i have been seeing notes here and there about Gene Therapy, and targeting FOXL2. introducing it into male mice.

Closest immediate things i have found while searching have been here: https://www.susans.org/forums/index.php?topic=156303.0

in which these two are refrenced: http://blogs.discovermagazine.com/notroc...to-minnie/http://www.healthline.com/health-news/te...lls-082613

 ---

Further research provided this: http://www.geneticsandsociety.org/article.php?id=5011

So to say its impossible. is nigh, just dangerous and needing more reasearch at the moment. - There is alot of inherient problems with gene therapy, as it causes changes at a rapid pace. Without Stem Cells, the repair of damaged nuclei is nearly impossible... Often resulting in cancer.(note all gene therapy) - This is why Stem Cell research is quite important. More importantly the research of Artificial Stem Cells. 
(https://www.sciencedaily.com/releases/20...134455.htm): Combined together Stem Cells and Gene Modification are like 2 peas in a pod, you could use it in this context to change, activate or induce a gene with ease. without the dangerous fallout.

----

My two cents and research.
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