Some students brought to my attention thier problems in studying parts of the Campos e Khamlichi reviews.
Please describe the main points of concern here, and we will try to explain and clarify.
Some students brought to my attention thier problems in studying parts of the Campos e Khamlichi reviews.
Please describe the main points of concern here, and we will try to explain and clarify.
Good evening, I post some questions about Khamlichi's Review:
1) X-inactivation is a RMAE which is defined as not so dependent on DNA methylation but during X-inactivation occurs CpG methylation at promoter of Xist in the active chromosome, induced by Tsix expression. So I do not understand if this process is strightly related to DNA methylation as described or not.
The problem remains open since to my knowledge there is no direct demonstration that CpG methylation at the Xist promoter is "causal" to transcriptional repression.
Co-localization of transcriptional repressors (e.g. HDACs) with DNMTs has been reported frequently, but cause-effect relationship has been sporadic, if any.
you may also see this old paper:
DOI: 10.1101/gad.10.16.1991I have other some problems with Campos'review:
1) I understood the role of nucleosomes about epigenetic inheritance and also the importance of histone modifiers such as PRC2, PRC1 and so on; the researchers say that in Drosophila those proteins can be maintained on chromatin during replication event through a looping mechanism which mediates interactions with regions ahead and behind replication fork: is this model sure or just a possibility? Moreover, I understood that in humans this event is not possible because there are not PREs and so is more probable that those proteins are displaced and then recruited after replication event, by contrast HP1 is likely maintained on chromatin thanks to interaction with CAF1 but I am not sure to have well understood this point.
2)About transmission of Epigenetic information through spermatogenesis: the most supported model is the retainment of some nucleosomes, but i don't understand if is possible that protamines may be involved in epigenetic propagation. If the answer is "Yes, they may be involved", is this pathway regulated by CHD5 which "transfers" PTMs from histones to protamines?
3)About reprogramming in the zygote: is the possible role of Bromodomain proteins to bookmark previously active genes in paternal loci and so to promote their re-activation after maternal-mediated reprogramming that occurs in the zygote?