Loading…

The histone variant H2A.W and linker histone H1 co-regulate heterochromatin accessibility and DNA methylation

Abstract In flowering plants, heterochromatin is demarcated by the histone variant H2A.W, elevated levels of the linker histone H1, and specific epigenetic modifications, such as high levels of DNA methylation at both CG and non-CG sites. How H2A.W regulates heterochromatin organization and interact...

Full description

Saved in:
Bibliographic Details
Published in:Nature communications 2021-12, Vol.12 (1)
Main Authors: Bourguet, Pierre, Picard, Colette, Yelagandula, Ramesh, Pélissier, Thierry, Lorković, Zdravko, Feng, Suhua, Pouch-Pélissier, Marie-Noëlle, Schmücker, Anna, Jacobsen, Steven, Berger, Frédéric, Mathieu, Olivier
Format: Article
Language:English
Subjects:
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by
cites
container_end_page
container_issue 1
container_start_page
container_title Nature communications
container_volume 12
creator Bourguet, Pierre
Picard, Colette
Yelagandula, Ramesh
Pélissier, Thierry
Lorković, Zdravko
Feng, Suhua
Pouch-Pélissier, Marie-Noëlle
Schmücker, Anna
Jacobsen, Steven
Berger, Frédéric
Mathieu, Olivier
description Abstract In flowering plants, heterochromatin is demarcated by the histone variant H2A.W, elevated levels of the linker histone H1, and specific epigenetic modifications, such as high levels of DNA methylation at both CG and non-CG sites. How H2A.W regulates heterochromatin organization and interacts with other heterochromatic features is unclear. Here, we create a h2a.w null mutant via CRISPR-Cas9, h2a.w-2 , to analyze the in vivo function of H2A.W. We find that H2A.W antagonizes deposition of H1 at heterochromatin and that non-CG methylation and accessibility are moderately decreased in h2a.w-2 heterochromatin. Compared to H1 loss alone, combined loss of H1 and H2A.W greatly increases accessibility and facilitates non-CG DNA methylation in heterochromatin, suggesting co-regulation of heterochromatic features by H2A.W and H1. Our results suggest that H2A.W helps maintain optimal heterochromatin accessibility and DNA methylation by promoting chromatin compaction together with H1, while also inhibiting excessive H1 incorporation.
doi_str_mv 10.1038/s41467-021-22993-5
format article
fullrecord <record><control><sourceid>hal</sourceid><recordid>TN_cdi_hal_primary_oai_HAL_hal_03375141v1</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>oai_HAL_hal_03375141v1</sourcerecordid><originalsourceid>FETCH-hal_primary_oai_HAL_hal_03375141v13</originalsourceid><addsrcrecordid>eNqVi8FKAzEURYNYsGh_wFW2LlLzktTpLAe1zEK6KnQ5PKfRPM0kksTC_L1jEXHr3dzL5RzGrkEuQer1bTZg7iohFQil6lqL1RmbK2lAQKX0-Z99wRY5v8kpuoa1MXM27JzljnKJwfIjJsJQeKua5Z5jOHBP4d2mX6AF3keR7OunxzJ5ttgUe5figIUCx763OdMzeSrjyX_YNnywxY0TTzFcsdkL-mwXP33JbjaPu_tWOPTdR6IB09hFpK5tnrrvT2pdrcDAEfR_2C9stlQk</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>The histone variant H2A.W and linker histone H1 co-regulate heterochromatin accessibility and DNA methylation</title><source>Publicly Available Content Database (Proquest) (PQ_SDU_P3)</source><source>Nature</source><source>PubMed Central</source><source>Springer Nature - nature.com Journals - Fully Open Access</source><creator>Bourguet, Pierre ; Picard, Colette ; Yelagandula, Ramesh ; Pélissier, Thierry ; Lorković, Zdravko ; Feng, Suhua ; Pouch-Pélissier, Marie-Noëlle ; Schmücker, Anna ; Jacobsen, Steven ; Berger, Frédéric ; Mathieu, Olivier</creator><creatorcontrib>Bourguet, Pierre ; Picard, Colette ; Yelagandula, Ramesh ; Pélissier, Thierry ; Lorković, Zdravko ; Feng, Suhua ; Pouch-Pélissier, Marie-Noëlle ; Schmücker, Anna ; Jacobsen, Steven ; Berger, Frédéric ; Mathieu, Olivier</creatorcontrib><description>Abstract In flowering plants, heterochromatin is demarcated by the histone variant H2A.W, elevated levels of the linker histone H1, and specific epigenetic modifications, such as high levels of DNA methylation at both CG and non-CG sites. How H2A.W regulates heterochromatin organization and interacts with other heterochromatic features is unclear. Here, we create a h2a.w null mutant via CRISPR-Cas9, h2a.w-2 , to analyze the in vivo function of H2A.W. We find that H2A.W antagonizes deposition of H1 at heterochromatin and that non-CG methylation and accessibility are moderately decreased in h2a.w-2 heterochromatin. Compared to H1 loss alone, combined loss of H1 and H2A.W greatly increases accessibility and facilitates non-CG DNA methylation in heterochromatin, suggesting co-regulation of heterochromatic features by H2A.W and H1. Our results suggest that H2A.W helps maintain optimal heterochromatin accessibility and DNA methylation by promoting chromatin compaction together with H1, while also inhibiting excessive H1 incorporation.</description><identifier>ISSN: 2041-1723</identifier><identifier>EISSN: 2041-1723</identifier><identifier>DOI: 10.1038/s41467-021-22993-5</identifier><language>eng</language><publisher>Nature Publishing Group</publisher><subject>Genetics ; Life Sciences</subject><ispartof>Nature communications, 2021-12, Vol.12 (1)</ispartof><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><orcidid>0000-0002-2177-2216 ; 0000-0001-7418-4322 ; 0000-0002-0213-0744 ; 0000-0002-2787-4360 ; 0000-0002-3609-8260 ; 0000-0001-5302-1102 ; 0000-0002-5019-4179 ; 0000-0002-3074-7258 ; 0000-0001-9483-138X ; 0000-0002-2177-2216 ; 0000-0002-3609-8260 ; 0000-0002-5019-4179 ; 0000-0002-0213-0744 ; 0000-0001-9483-138X ; 0000-0001-5302-1102 ; 0000-0001-7418-4322 ; 0000-0002-2787-4360 ; 0000-0002-3074-7258</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://hal.science/hal-03375141$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Bourguet, Pierre</creatorcontrib><creatorcontrib>Picard, Colette</creatorcontrib><creatorcontrib>Yelagandula, Ramesh</creatorcontrib><creatorcontrib>Pélissier, Thierry</creatorcontrib><creatorcontrib>Lorković, Zdravko</creatorcontrib><creatorcontrib>Feng, Suhua</creatorcontrib><creatorcontrib>Pouch-Pélissier, Marie-Noëlle</creatorcontrib><creatorcontrib>Schmücker, Anna</creatorcontrib><creatorcontrib>Jacobsen, Steven</creatorcontrib><creatorcontrib>Berger, Frédéric</creatorcontrib><creatorcontrib>Mathieu, Olivier</creatorcontrib><title>The histone variant H2A.W and linker histone H1 co-regulate heterochromatin accessibility and DNA methylation</title><title>Nature communications</title><description>Abstract In flowering plants, heterochromatin is demarcated by the histone variant H2A.W, elevated levels of the linker histone H1, and specific epigenetic modifications, such as high levels of DNA methylation at both CG and non-CG sites. How H2A.W regulates heterochromatin organization and interacts with other heterochromatic features is unclear. Here, we create a h2a.w null mutant via CRISPR-Cas9, h2a.w-2 , to analyze the in vivo function of H2A.W. We find that H2A.W antagonizes deposition of H1 at heterochromatin and that non-CG methylation and accessibility are moderately decreased in h2a.w-2 heterochromatin. Compared to H1 loss alone, combined loss of H1 and H2A.W greatly increases accessibility and facilitates non-CG DNA methylation in heterochromatin, suggesting co-regulation of heterochromatic features by H2A.W and H1. Our results suggest that H2A.W helps maintain optimal heterochromatin accessibility and DNA methylation by promoting chromatin compaction together with H1, while also inhibiting excessive H1 incorporation.</description><subject>Genetics</subject><subject>Life Sciences</subject><issn>2041-1723</issn><issn>2041-1723</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><recordid>eNqVi8FKAzEURYNYsGh_wFW2LlLzktTpLAe1zEK6KnQ5PKfRPM0kksTC_L1jEXHr3dzL5RzGrkEuQer1bTZg7iohFQil6lqL1RmbK2lAQKX0-Z99wRY5v8kpuoa1MXM27JzljnKJwfIjJsJQeKua5Z5jOHBP4d2mX6AF3keR7OunxzJ5ttgUe5figIUCx763OdMzeSrjyX_YNnywxY0TTzFcsdkL-mwXP33JbjaPu_tWOPTdR6IB09hFpK5tnrrvT2pdrcDAEfR_2C9stlQk</recordid><startdate>202112</startdate><enddate>202112</enddate><creator>Bourguet, Pierre</creator><creator>Picard, Colette</creator><creator>Yelagandula, Ramesh</creator><creator>Pélissier, Thierry</creator><creator>Lorković, Zdravko</creator><creator>Feng, Suhua</creator><creator>Pouch-Pélissier, Marie-Noëlle</creator><creator>Schmücker, Anna</creator><creator>Jacobsen, Steven</creator><creator>Berger, Frédéric</creator><creator>Mathieu, Olivier</creator><general>Nature Publishing Group</general><scope>1XC</scope><scope>VOOES</scope><orcidid>https://orcid.org/0000-0002-2177-2216</orcidid><orcidid>https://orcid.org/0000-0001-7418-4322</orcidid><orcidid>https://orcid.org/0000-0002-0213-0744</orcidid><orcidid>https://orcid.org/0000-0002-2787-4360</orcidid><orcidid>https://orcid.org/0000-0002-3609-8260</orcidid><orcidid>https://orcid.org/0000-0001-5302-1102</orcidid><orcidid>https://orcid.org/0000-0002-5019-4179</orcidid><orcidid>https://orcid.org/0000-0002-3074-7258</orcidid><orcidid>https://orcid.org/0000-0001-9483-138X</orcidid><orcidid>https://orcid.org/0000-0002-2177-2216</orcidid><orcidid>https://orcid.org/0000-0002-3609-8260</orcidid><orcidid>https://orcid.org/0000-0002-5019-4179</orcidid><orcidid>https://orcid.org/0000-0002-0213-0744</orcidid><orcidid>https://orcid.org/0000-0001-9483-138X</orcidid><orcidid>https://orcid.org/0000-0001-5302-1102</orcidid><orcidid>https://orcid.org/0000-0001-7418-4322</orcidid><orcidid>https://orcid.org/0000-0002-2787-4360</orcidid><orcidid>https://orcid.org/0000-0002-3074-7258</orcidid></search><sort><creationdate>202112</creationdate><title>The histone variant H2A.W and linker histone H1 co-regulate heterochromatin accessibility and DNA methylation</title><author>Bourguet, Pierre ; Picard, Colette ; Yelagandula, Ramesh ; Pélissier, Thierry ; Lorković, Zdravko ; Feng, Suhua ; Pouch-Pélissier, Marie-Noëlle ; Schmücker, Anna ; Jacobsen, Steven ; Berger, Frédéric ; Mathieu, Olivier</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-hal_primary_oai_HAL_hal_03375141v13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Genetics</topic><topic>Life Sciences</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bourguet, Pierre</creatorcontrib><creatorcontrib>Picard, Colette</creatorcontrib><creatorcontrib>Yelagandula, Ramesh</creatorcontrib><creatorcontrib>Pélissier, Thierry</creatorcontrib><creatorcontrib>Lorković, Zdravko</creatorcontrib><creatorcontrib>Feng, Suhua</creatorcontrib><creatorcontrib>Pouch-Pélissier, Marie-Noëlle</creatorcontrib><creatorcontrib>Schmücker, Anna</creatorcontrib><creatorcontrib>Jacobsen, Steven</creatorcontrib><creatorcontrib>Berger, Frédéric</creatorcontrib><creatorcontrib>Mathieu, Olivier</creatorcontrib><collection>Hyper Article en Ligne (HAL)</collection><collection>Hyper Article en Ligne (HAL) (Open Access)</collection><jtitle>Nature communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bourguet, Pierre</au><au>Picard, Colette</au><au>Yelagandula, Ramesh</au><au>Pélissier, Thierry</au><au>Lorković, Zdravko</au><au>Feng, Suhua</au><au>Pouch-Pélissier, Marie-Noëlle</au><au>Schmücker, Anna</au><au>Jacobsen, Steven</au><au>Berger, Frédéric</au><au>Mathieu, Olivier</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The histone variant H2A.W and linker histone H1 co-regulate heterochromatin accessibility and DNA methylation</atitle><jtitle>Nature communications</jtitle><date>2021-12</date><risdate>2021</risdate><volume>12</volume><issue>1</issue><issn>2041-1723</issn><eissn>2041-1723</eissn><abstract>Abstract In flowering plants, heterochromatin is demarcated by the histone variant H2A.W, elevated levels of the linker histone H1, and specific epigenetic modifications, such as high levels of DNA methylation at both CG and non-CG sites. How H2A.W regulates heterochromatin organization and interacts with other heterochromatic features is unclear. Here, we create a h2a.w null mutant via CRISPR-Cas9, h2a.w-2 , to analyze the in vivo function of H2A.W. We find that H2A.W antagonizes deposition of H1 at heterochromatin and that non-CG methylation and accessibility are moderately decreased in h2a.w-2 heterochromatin. Compared to H1 loss alone, combined loss of H1 and H2A.W greatly increases accessibility and facilitates non-CG DNA methylation in heterochromatin, suggesting co-regulation of heterochromatic features by H2A.W and H1. Our results suggest that H2A.W helps maintain optimal heterochromatin accessibility and DNA methylation by promoting chromatin compaction together with H1, while also inhibiting excessive H1 incorporation.</abstract><pub>Nature Publishing Group</pub><doi>10.1038/s41467-021-22993-5</doi><orcidid>https://orcid.org/0000-0002-2177-2216</orcidid><orcidid>https://orcid.org/0000-0001-7418-4322</orcidid><orcidid>https://orcid.org/0000-0002-0213-0744</orcidid><orcidid>https://orcid.org/0000-0002-2787-4360</orcidid><orcidid>https://orcid.org/0000-0002-3609-8260</orcidid><orcidid>https://orcid.org/0000-0001-5302-1102</orcidid><orcidid>https://orcid.org/0000-0002-5019-4179</orcidid><orcidid>https://orcid.org/0000-0002-3074-7258</orcidid><orcidid>https://orcid.org/0000-0001-9483-138X</orcidid><orcidid>https://orcid.org/0000-0002-2177-2216</orcidid><orcidid>https://orcid.org/0000-0002-3609-8260</orcidid><orcidid>https://orcid.org/0000-0002-5019-4179</orcidid><orcidid>https://orcid.org/0000-0002-0213-0744</orcidid><orcidid>https://orcid.org/0000-0001-9483-138X</orcidid><orcidid>https://orcid.org/0000-0001-5302-1102</orcidid><orcidid>https://orcid.org/0000-0001-7418-4322</orcidid><orcidid>https://orcid.org/0000-0002-2787-4360</orcidid><orcidid>https://orcid.org/0000-0002-3074-7258</orcidid><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 2041-1723
ispartof Nature communications, 2021-12, Vol.12 (1)
issn 2041-1723
2041-1723
language eng
recordid cdi_hal_primary_oai_HAL_hal_03375141v1
source Publicly Available Content Database (Proquest) (PQ_SDU_P3); Nature; PubMed Central; Springer Nature - nature.com Journals - Fully Open Access
subjects Genetics
Life Sciences
title The histone variant H2A.W and linker histone H1 co-regulate heterochromatin accessibility and DNA methylation
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-27T13%3A27%3A11IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-hal&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=The%20histone%20variant%20H2A.W%20and%20linker%20histone%20H1%20co-regulate%20heterochromatin%20accessibility%20and%20DNA%20methylation&rft.jtitle=Nature%20communications&rft.au=Bourguet,%20Pierre&rft.date=2021-12&rft.volume=12&rft.issue=1&rft.issn=2041-1723&rft.eissn=2041-1723&rft_id=info:doi/10.1038/s41467-021-22993-5&rft_dat=%3Chal%3Eoai_HAL_hal_03375141v1%3C/hal%3E%3Cgrp_id%3Ecdi_FETCH-hal_primary_oai_HAL_hal_03375141v13%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_id=info:pmid/&rfr_iscdi=true