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Transcriptional repression by PRC1 in the absence of H2A monoubiquitylation
Histone H2A monoubiquitylation (H2Aub) is considered to be a key effector in transcriptional repression by Polycomb-repressive complex 1 (PRC1). We analyzed Drosophila with a point mutation in the PRC1 subunit Sce that abolishes its H2A ubiquitylase activity or with point mutations in the H2A and H2...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Cold Spring Harbor Laboratory Press
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4526733/ https://www.ncbi.nlm.nih.gov/pubmed/26178786 http://dx.doi.org/10.1101/gad.265439.115 |
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author | Pengelly, Ana Raquel Kalb, Reinhard Finkl, Katja Müller, Jürg |
author_facet | Pengelly, Ana Raquel Kalb, Reinhard Finkl, Katja Müller, Jürg |
author_sort | Pengelly, Ana Raquel |
collection | PubMed |
description | Histone H2A monoubiquitylation (H2Aub) is considered to be a key effector in transcriptional repression by Polycomb-repressive complex 1 (PRC1). We analyzed Drosophila with a point mutation in the PRC1 subunit Sce that abolishes its H2A ubiquitylase activity or with point mutations in the H2A and H2Av residues ubiquitylated by PRC1. H2Aub is essential for viability and required for efficient histone H3 Lys27 trimethylation by PRC2 early in embryogenesis. However, H2Aub-deficient animals fully maintain repression of PRC1 target genes and do not show phenotypes characteristic of Polycomb group mutants. PRC1 thus represses canonical target genes independently of H2Aub. |
format | Online Article Text |
id | pubmed-4526733 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Cold Spring Harbor Laboratory Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-45267332016-01-15 Transcriptional repression by PRC1 in the absence of H2A monoubiquitylation Pengelly, Ana Raquel Kalb, Reinhard Finkl, Katja Müller, Jürg Genes Dev Research Communication Histone H2A monoubiquitylation (H2Aub) is considered to be a key effector in transcriptional repression by Polycomb-repressive complex 1 (PRC1). We analyzed Drosophila with a point mutation in the PRC1 subunit Sce that abolishes its H2A ubiquitylase activity or with point mutations in the H2A and H2Av residues ubiquitylated by PRC1. H2Aub is essential for viability and required for efficient histone H3 Lys27 trimethylation by PRC2 early in embryogenesis. However, H2Aub-deficient animals fully maintain repression of PRC1 target genes and do not show phenotypes characteristic of Polycomb group mutants. PRC1 thus represses canonical target genes independently of H2Aub. Cold Spring Harbor Laboratory Press 2015-07-15 /pmc/articles/PMC4526733/ /pubmed/26178786 http://dx.doi.org/10.1101/gad.265439.115 Text en © 2015 Pengelly et al.; Published by Cold Spring Harbor Laboratory Press http://creativecommons.org/licenses/by-nc/4.0/ This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/. |
spellingShingle | Research Communication Pengelly, Ana Raquel Kalb, Reinhard Finkl, Katja Müller, Jürg Transcriptional repression by PRC1 in the absence of H2A monoubiquitylation |
title | Transcriptional repression by PRC1 in the absence of H2A monoubiquitylation |
title_full | Transcriptional repression by PRC1 in the absence of H2A monoubiquitylation |
title_fullStr | Transcriptional repression by PRC1 in the absence of H2A monoubiquitylation |
title_full_unstemmed | Transcriptional repression by PRC1 in the absence of H2A monoubiquitylation |
title_short | Transcriptional repression by PRC1 in the absence of H2A monoubiquitylation |
title_sort | transcriptional repression by prc1 in the absence of h2a monoubiquitylation |
topic | Research Communication |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4526733/ https://www.ncbi.nlm.nih.gov/pubmed/26178786 http://dx.doi.org/10.1101/gad.265439.115 |
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