I hope I'll be able to understand all this bunch of infos after the first dozen of times that I watch it thoroughly. Thanks for uploading the result of your hard work. Best wishes!
I think that this is not the whole story. Cus we should know under what basics the whole chromosome silence took place and why in some germ cells the deactivation is for the mom x and other for dad x . And we need extra light on partial deactivation of the x chromosome which permits some of the genes working. Regards to that scientific work that simplifies the solid scientific subjects Shreiner Aly
Now, as I read about Prof. jeannie T. Lee PhD research focused on Fragile X syndrome, I'd like to comment on my theory to (maybe) explain why and how strong Phosphodiester bonds are broken. Breakpoint clusters are palindromic, just like the regions of bacteriophages genomes that are targeted by restriction enzymes ; I think that nucleases (possibly produced by bacteria as restriction enzymes against bacteriophages) released in the cytoplasm could reach palindromic regions of the DNA in the nucleus at the end of prophase.
By 18:42 I became curious to know if all this vast research made it possible to understand how the methilation of the inactivated X chromossomes, that supposedly should silence most (if not all) genes, may be related to the increased number of cancers that are prevalent in women and are somehow originated in the SILENCED, inactivated X chromosome and not in the active chromosome of a somatic cell of a female. Perhaps the proofreading from DNA polymerase just can't reach such methilated X chromosomes...
So, does ctcf contribute in repression or expression of xist (at the end she mentioned that ctcf down regulates tsix thereby activating xist; before this when she mentioned about jpx, she said that ctcf blocks/represses xist expression and is only initiated when jpx removes ctcf by binding to ctcf;) but thank you ma'am for the lecture 🩷☺️
