The Polycomb group protein EED is dispensable for the initiation of random X-chromosome inactivation.

The Polycomb group (PcG) proteins are thought to silence gene expression by modifying chromatin. The Polycomb repressive complex 2 (PRC2) plays an essential role in mammalian X-chromosome inactivation (XCI), a model system to investigate heritable gene silencing. In the mouse, two different forms of...

Full description

Saved in:
Bibliographic Details
Main Authors: Sundeep Kalantry, Terry Magnuson
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2006-05-01
Series:PLoS Genetics
Online Access:https://journals.plos.org/plosgenetics/article/file?id=10.1371/journal.pgen.0020066&type=printable
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1841533258236428288
author Sundeep Kalantry
Terry Magnuson
author_facet Sundeep Kalantry
Terry Magnuson
author_sort Sundeep Kalantry
collection DOAJ
description The Polycomb group (PcG) proteins are thought to silence gene expression by modifying chromatin. The Polycomb repressive complex 2 (PRC2) plays an essential role in mammalian X-chromosome inactivation (XCI), a model system to investigate heritable gene silencing. In the mouse, two different forms of XCI occur. In the preimplantation embryo, all cells undergo imprinted inactivation of the paternal X-chromosome (Xp). During the peri-implantation period, cells destined to give rise to the embryo proper erase the imprint and randomly inactivate either the maternal X-chromosome or the Xp; extraembryonic cells, on the other hand, maintain imprinted XCI of the Xp. PRC2 proteins are enriched on the inactive-X during early stages of both imprinted and random XCI. It is therefore thought that PRC2 contributes to the initiation of XCI. Mouse embryos lacking the essential PRC2 component EED harbor defects in the maintenance of imprinted XCI in differentiating trophoblast cells. Assessment of PRC2 requirement in the initiation of XCI, however, has been hindered by the presence of maternally derived proteins in the early embryo. Here we show that Eed-/- embryos initiate and maintain random XCI despite lacking any functional EED protein prior to the initiation of random XCI. Thus, despite being enriched on the inactive X-chromosome, PcGs appear to be dispensable for the initiation and maintenance of random XCI. These results highlight the lineage- and differentiation state-specific requirements for PcGs in XCI and argue against PcG function in the formation of the facultative heterochromatin of the inactive X-chromosome.
format Article
id doaj-art-b86e7d6478db4d1b8ab235351325b7a6
institution Kabale University
issn 1553-7390
1553-7404
language English
publishDate 2006-05-01
publisher Public Library of Science (PLoS)
record_format Article
series PLoS Genetics
spelling doaj-art-b86e7d6478db4d1b8ab235351325b7a62025-01-17T05:31:15ZengPublic Library of Science (PLoS)PLoS Genetics1553-73901553-74042006-05-0125e6610.1371/journal.pgen.0020066The Polycomb group protein EED is dispensable for the initiation of random X-chromosome inactivation.Sundeep KalantryTerry MagnusonThe Polycomb group (PcG) proteins are thought to silence gene expression by modifying chromatin. The Polycomb repressive complex 2 (PRC2) plays an essential role in mammalian X-chromosome inactivation (XCI), a model system to investigate heritable gene silencing. In the mouse, two different forms of XCI occur. In the preimplantation embryo, all cells undergo imprinted inactivation of the paternal X-chromosome (Xp). During the peri-implantation period, cells destined to give rise to the embryo proper erase the imprint and randomly inactivate either the maternal X-chromosome or the Xp; extraembryonic cells, on the other hand, maintain imprinted XCI of the Xp. PRC2 proteins are enriched on the inactive-X during early stages of both imprinted and random XCI. It is therefore thought that PRC2 contributes to the initiation of XCI. Mouse embryos lacking the essential PRC2 component EED harbor defects in the maintenance of imprinted XCI in differentiating trophoblast cells. Assessment of PRC2 requirement in the initiation of XCI, however, has been hindered by the presence of maternally derived proteins in the early embryo. Here we show that Eed-/- embryos initiate and maintain random XCI despite lacking any functional EED protein prior to the initiation of random XCI. Thus, despite being enriched on the inactive X-chromosome, PcGs appear to be dispensable for the initiation and maintenance of random XCI. These results highlight the lineage- and differentiation state-specific requirements for PcGs in XCI and argue against PcG function in the formation of the facultative heterochromatin of the inactive X-chromosome.https://journals.plos.org/plosgenetics/article/file?id=10.1371/journal.pgen.0020066&type=printable
spellingShingle Sundeep Kalantry
Terry Magnuson
The Polycomb group protein EED is dispensable for the initiation of random X-chromosome inactivation.
PLoS Genetics
title The Polycomb group protein EED is dispensable for the initiation of random X-chromosome inactivation.
title_full The Polycomb group protein EED is dispensable for the initiation of random X-chromosome inactivation.
title_fullStr The Polycomb group protein EED is dispensable for the initiation of random X-chromosome inactivation.
title_full_unstemmed The Polycomb group protein EED is dispensable for the initiation of random X-chromosome inactivation.
title_short The Polycomb group protein EED is dispensable for the initiation of random X-chromosome inactivation.
title_sort polycomb group protein eed is dispensable for the initiation of random x chromosome inactivation
url https://journals.plos.org/plosgenetics/article/file?id=10.1371/journal.pgen.0020066&type=printable
work_keys_str_mv AT sundeepkalantry thepolycombgroupproteineedisdispensablefortheinitiationofrandomxchromosomeinactivation
AT terrymagnuson thepolycombgroupproteineedisdispensablefortheinitiationofrandomxchromosomeinactivation
AT sundeepkalantry polycombgroupproteineedisdispensablefortheinitiationofrandomxchromosomeinactivation
AT terrymagnuson polycombgroupproteineedisdispensablefortheinitiationofrandomxchromosomeinactivation