Posted: Jan 15, 2018 10:58 pm
Primary sexual features - testes or ovaries - actually appear early in the foetal developmental cycle, and indeed, are needed for this, so that certain secondary sexual features can develop. This is because important secondary sexual features - whether or not you have a penis or a vagina when you are born - are heavily dependent upon testosterone and androgen being generated by the testes, to stimulate the androgen receptors into male pattern development. Female pattern development takes place in the absence of androgen receptor stimulation by testosterone and androgen. See CAIS for what happens when this fails to operate as usual, due to mutations in the androgen receptor gene.
The interesting part is that in some mammals (principally rodents), nipple buds develop early in the foetal developmental cycle, but a separate signalling system based upon parathyroid hormone related protein (PTHrP), determines whether the nipple buds will develop further, or atrophy. PTHrP stimulates the nipple bud cells, as they divide, to express androgen receptors on their surface. If those androgen receptors are then triggered, male pattern development ensues, as above, and in the case of rodents, the nipples disappear altogether. If the androgen receptors are not triggered, female pattern development ensues, and the nipples continue growing.
In humans, it appears that the "shutdown" program, so to speak, is either incomplete or has been turned off, and this is also the case for many other mammals, so males in these species have visible nipples. The BMP4 protein also plays a role in nipple bud development (indeed, BMP4 crops up pretty much ubiquitously in development - it's found in bone, tooth and organ development pathways right across the development spectrum), and in turn recruits the Msx2 signalling pathway. The Msx2 pathway is the pathway that results in androgen receptor expression on nipple bud cells.
I'll have to delve into the literature in more detail to find out what's going on, but it appears the androgen receptors playing a role in penis/vagina differentiation, are important players in nipple development too.
The interesting part is that in some mammals (principally rodents), nipple buds develop early in the foetal developmental cycle, but a separate signalling system based upon parathyroid hormone related protein (PTHrP), determines whether the nipple buds will develop further, or atrophy. PTHrP stimulates the nipple bud cells, as they divide, to express androgen receptors on their surface. If those androgen receptors are then triggered, male pattern development ensues, as above, and in the case of rodents, the nipples disappear altogether. If the androgen receptors are not triggered, female pattern development ensues, and the nipples continue growing.
In humans, it appears that the "shutdown" program, so to speak, is either incomplete or has been turned off, and this is also the case for many other mammals, so males in these species have visible nipples. The BMP4 protein also plays a role in nipple bud development (indeed, BMP4 crops up pretty much ubiquitously in development - it's found in bone, tooth and organ development pathways right across the development spectrum), and in turn recruits the Msx2 signalling pathway. The Msx2 pathway is the pathway that results in androgen receptor expression on nipple bud cells.
I'll have to delve into the literature in more detail to find out what's going on, but it appears the androgen receptors playing a role in penis/vagina differentiation, are important players in nipple development too.