What makes the maternal X chromosome resistant to undergoing imprinted X inactivation?

Abstract

In the mouse, while either X chromosome is chosen for inactivation in a random fashion in the embryonic tissue, the paternally derived X chromosome is preferentially inactivated in the extraembryonic tissues. It has been shown that the maternal X chromosome is imprinted so as not to undergo inactivation in the extraembryonic tissues. X-linked noncoding RNA becomes upregulated on the X chromosome that is to be inactivated. An antisense noncoding RNA,, which occurs at the locus and has been shown to negatively regulate expression in cis, is imprinted to be expressed from the maternal X in the extraembryonic tissues. Although appears to be responsible for the imprint laid on the maternal X, those who disagree with this idea would point out the fact that has not yet been expressed from the maternal X when becomes upregulated on the paternal but not the maternal X at the onset of imprinted X-inactivation in preimplantation embryos. Recent studies have demonstrated, however, that there is a prominent difference in the chromatin structure at the locus depending on the parental origin, which I suggest might account for the repression of maternal in the absence of maternal at the preimplantation stages.This article is part of the themed issue 'X-chromosome inactivation: a tribute to Mary Lyon'.

Mechanisms of Choice in X-Chromosome Inactivation

“…The absence of imprinted Xist expression in non-rodent eutherian species, which in general have a later onset of XCI in early development, has been suggested to be linked to the fact that embryos of those species undergo several rounds of DNA replication before Xist starts to be expressed; this way, parent-specific chromatin structure differences would possibly be erased, resulting in the two Xist alleles being epigenetically identical [74,75]. A more recent model posits that an imprint that instructs strictly monoallelic XCI must exist in species with early XCI initiation (such as marsupials and mice) to prevent the possibility of inactivating both X chromosomes [68], which, nevertheless, happens during random XCI (discussed below).…”

Sex Determination in Homo sapiens as a Multi-Step Process: Potential for Development of Variants and Sex Differences in Disease Risk

“…As the X chromosome contains ~800 genes, versus ~60 on the Y chromosome [22], it therefore contains a large number of sex-defining genes affecting a variety of tissues [discussed in [21]]. As a female obtains an X chromosome from both the sperm donor and the egg donor at the time of conception, one X chromosome is inactivated in different tissues either randomly or selectively [23][24][25][26][27], giving rise to mosaic expression patterns.…”

Mechanisms of Choice in X-Chromosome Inactivation

“…The absence of imprinted Xist expression in non-rodent eutherian species, which in general have a later onset of XCI in early development, has been suggested to be linked to the fact that embryos of those species undergo several rounds of DNA replication before Xist starts to be expressed; this way, parent-specific chromatin structure differences would possibly be erased, resulting in the two Xist alleles being epigenetically identical (Sado, 2017;Sado and Sakaguchi, 2013). A more recent model posits that an imprint that instructs strictly monoallelic XCI must exist in species with early XCI initiation (such as marsupials and mice) to prevent the possibility of inactivating both X chromosomes (Mahadevaiah et al, 2020), which, nevertheless, sometimes happens during random XCI (discussed below).…”