Electronics Engineering, AI Research / @_cantelli 
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Male mice grow ovaries & female genitalia instead of testes if they are missing a small region of non-coding DNA. Deleting an element of Sox9 gives rise to XY's (probably critical in humans), with full development of ovaries and female genitalia. http://science.sciencemag.org/content/early/2018/06/13/science.aas9408 …pic.twitter.com/1fyxS7ovyy
Clarification:The XT Enh13-/- females here went into full development and were born and are still alive. They are complete females, however they are unable to reproduce, they are infertile. The same applies human patients that are born as XY females — they are also all infertile
This is the also case of all XY females that were ever formed using mutations in different genes (SRY for example, or Enh13 like it has been shown here). They have ovaries, genitalia, but they are unable to produce normal oocytes.
These kinds of things make you realize how tiny differences can easily make a big impact. Makes you wonder about the "not enough variation" argument re race differences...
Yes, if one considers that non-additive epistatic interactions can contribute to genetic variance components, then a cascade domino effect similar to sexual development can unlock enough variation for race differences. In Drosophila: http://www.pnas.org/content/112/27/E3555 …pic.twitter.com/nci6Z4r3PX
I should think most of the race things are going to be small parameter differences in promoter regions. Turn this pathway up 5%, this other one down 10%, kind of thing.
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