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Philos Trans R Soc Lond B Biol Sci. 2017 Nov 5;372(1733). pii: 20160363. doi: 10.1098/rstb.2016.0363.

Regulation of X-chromosome dosage compensation in human: mechanisms and model systems.

Author information

1
David Geffen School of Medicine, Department of Biological Chemistry, Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, Jonsson Comprehensive Cancer Center, Molecular Biology Institute, University of California Los Angeles, Los Angeles, CA 90095, USA.
2
David Geffen School of Medicine, Department of Biological Chemistry, Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, Jonsson Comprehensive Cancer Center, Molecular Biology Institute, University of California Los Angeles, Los Angeles, CA 90095, USA kplath@mednet.ucla.edu.
3
Sorbonne Paris Cité, Epigenetics and Cell Fate, UMR 7216 CNRS, Université Paris Diderot, Paris, France.

Abstract

The human blastocyst forms 5 days after one of the smallest human cells (the sperm) fertilizes one of the largest human cells (the egg). Depending on the sex-chromosome contribution from the sperm, the resulting embryo will either be female, with two X chromosomes (XX), or male, with an X and a Y chromosome (XY). In early development, one of the major differences between XX female and XY male embryos is the conserved process of X-chromosome inactivation (XCI), which compensates gene expression of the two female X chromosomes to match the dosage of the single X chromosome of males. Most of our understanding of the pre-XCI state and XCI establishment is based on mouse studies, but recent evidence from human pre-implantation embryo research suggests that many of the molecular steps defined in the mouse are not conserved in human. Here, we will discuss recent advances in understanding the control of X-chromosome dosage compensation in early human embryonic development and compare it to that of the mouse.This article is part of the themed issue 'X-chromosome inactivation: a tribute to Mary Lyon'.

KEYWORDS:

X-chromosome dampening; X-chromosome inactivation; Xact; Xist; pluripotent stem cells

PMID:
28947660
PMCID:
PMC5627163
DOI:
10.1098/rstb.2016.0363
[Indexed for MEDLINE]
Free PMC Article

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