scholarly journals The role of Xist in the regulation of X chromosome inactivation

1998 ◽  
Vol 72 (1) ◽  
pp. 59-72
Author(s):  
COLETTE M. JOHNSTON ◽  
SARAH M. DUTHIE ◽  
STEVEN A. SHEARDOWN ◽  
ALISTAIR E. T. NEWALL ◽  
EMMA J. FORMSTONE ◽  
...  
2006 ◽  
Vol 2006 ◽  
pp. 1-6 ◽  
Author(s):  
Mary F. Lyon

There is longstanding evidence that X-chromosome inactivation (XCI) travels less successfully in autosomal than in X-chromosomal chromatin. The interspersed repeat elements LINE1s (L1s) have been suggested as candidates for “boosters” which promote the spread of XCI in the X-chromosome. The present paper reviews the current evidence concerning the possible role of L1s in XCI. Recent evidence, accruing from the human genome sequencing project and other sources, confirms that mammalian X-chromosomes are indeed rich in L1s, except in regions where there are many genes escaping XCI. The density of L1s is the highest in the evolutionarily oldest regions. Recent work on X; autosome translocations in human and mouse suggested failure of stabilization of XCI in autosomal material, so that genes are reactivated, but resistance of autosomal genes to the original silencing is not excluded. The accumulation of L1s on the X-chromosome may have resulted from reduced recombination or late replication. Whether L1s are part of the mechanism of XCI or a result of it remains enigmatic.


2004 ◽  
Vol 2 (1) ◽  
pp. 27-37
Author(s):  
Anna A Pendina ◽  
Vera V Grinkevich ◽  
Tatyana V Kuznetsova ◽  
Vladislav S Baranov

 DNA methylation is one of the main mechanisms of epigenetic inheritance in eukaryotes. In this review we looked through the ways of 5-methylcytosin origin, it's distribution in genome, the mechanism of gene repression via hypermetilation, the role of metylation in genomic imprinting and in X-chromosome inactivation, in embryogenesis of mammals, in the processes of oncogenesis and in etiology of some common human inherited diseases


Genetics ◽  
2019 ◽  
Vol 213 (2) ◽  
pp. 685-703
Author(s):  
Chen-Yu Wang ◽  
Harrison Brand ◽  
Natalie D. Shaw ◽  
Michael E. Talkowski ◽  
Jeannie T. Lee

2021 ◽  
Author(s):  
Iromi Wanigasuriya ◽  
Sarah A Kinkel ◽  
Tamara Beck ◽  
Ellise A Roper ◽  
Kelsey Breslin ◽  
...  

Embryonic development is dependent on the maternal supply of proteins through the oocyte, including factors setting up the adequate epigenetic patterning of the zygotic genome. We previously reported that one such factor is the epigenetic repressor SMCHD1, whose maternal supply controls autosomal imprinted expression in mouse preimplantation embryos and mid-gestation placenta. In mouse preimplantation embryos, X chromosome inactivation is also an imprinted process. Combining genomics and imaging, we show that maternal SMCHD1 is required not only for the imprinted expression of Xist in preimplantation embryos, but also for the efficient silencing of the inactive X in both the preimplantation embryo and mid-gestation placenta. These results expand the role of SMCHD1 in enforcing the silencing of Polycomb targets. The inability of zygotic SMCHD1 to fully restore imprinted X inactivation further points to maternal SMCHD1's role in setting up the appropriate chromatin environment during preimplantation development, a critical window of epigenetic remodelling.


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