Set2‐mediated H3K36 methylation states redundantly repress the production of antisense transcripts: role in transcription regulation

Methyltransferase Set2‐mediated methylation of histone H3 lysine 36 (H3K36), which involves the addition of up to three methyl groups at this site, has been demonstrated to function in many chromatin‐coupled events. The methylation of H3K36 is known to recruit different chromatin effector proteins,...

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Main Authors: Yu‐Chao Mei, Jiangpeng Feng, Fei He, Yu‐Min Li, Yafei Liu, Feng Li, Yu Chen, Hai‐Ning Du
Format: Article
Language:English
Published: Wiley 2021-08-01
Series:FEBS Open Bio
Subjects:
Online Access:https://doi.org/10.1002/2211-5463.13226
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author Yu‐Chao Mei
Jiangpeng Feng
Fei He
Yu‐Min Li
Yafei Liu
Feng Li
Yu Chen
Hai‐Ning Du
author_facet Yu‐Chao Mei
Jiangpeng Feng
Fei He
Yu‐Min Li
Yafei Liu
Feng Li
Yu Chen
Hai‐Ning Du
author_sort Yu‐Chao Mei
collection DOAJ
description Methyltransferase Set2‐mediated methylation of histone H3 lysine 36 (H3K36), which involves the addition of up to three methyl groups at this site, has been demonstrated to function in many chromatin‐coupled events. The methylation of H3K36 is known to recruit different chromatin effector proteins, affecting transcription, mRNA splicing and DNA repair. In this study, we engineered two yeast set2 mutants that lack H3K36 mono/dimethylation (H3K36me1/2) and trimethylation (H3K36me3), respectively, and characterized their roles in the production of antisense transcripts under nutrient‐rich conditions. Using our new bioinformatics identification pipeline analysis, we are able to identify a larger number of antisense transcripts in set2∆ cells than has been published previously. We further show that H3K36me1/2 or H3K36me3 redundantly repressed the production of antisense transcripts. Moreover, gene ontology (GO) analysis implies that H3K36me3‐mediated antisense transcription might play a role in DNA replication and DNA damage repair, which is independent of regulation of the corresponding sense gene expression. Overall, our results validate a coregulatory mechanism of different H3K36 methylation states, particularly in the repression of antisense transcription.
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spelling doaj.art-8e971fa348704ae48c07d96bc6f5b2562023-07-04T10:16:02ZengWileyFEBS Open Bio2211-54632021-08-011182225223510.1002/2211-5463.13226Set2‐mediated H3K36 methylation states redundantly repress the production of antisense transcripts: role in transcription regulationYu‐Chao Mei0Jiangpeng Feng1Fei He2Yu‐Min Li3Yafei Liu4Feng Li5Yu Chen6Hai‐Ning Du7Hubei Key Laboratory of Cell Homeostasis College of Life Sciences RNA Institute Wuhan University ChinaState Key Laboratory of Virology College of Life Sciences RNA Institute Wuhan University ChinaState Key Laboratory of Biocatalysis and Enzyme Engineering School of Life Sciences Hubei University Wuhan ChinaHubei Key Laboratory of Cell Homeostasis College of Life Sciences RNA Institute Wuhan University ChinaHubei Key Laboratory of Cell Homeostasis College of Life Sciences RNA Institute Wuhan University ChinaSchool of Basic Medical Sciences Wuhan University ChinaState Key Laboratory of Virology College of Life Sciences RNA Institute Wuhan University ChinaHubei Key Laboratory of Cell Homeostasis College of Life Sciences RNA Institute Wuhan University ChinaMethyltransferase Set2‐mediated methylation of histone H3 lysine 36 (H3K36), which involves the addition of up to three methyl groups at this site, has been demonstrated to function in many chromatin‐coupled events. The methylation of H3K36 is known to recruit different chromatin effector proteins, affecting transcription, mRNA splicing and DNA repair. In this study, we engineered two yeast set2 mutants that lack H3K36 mono/dimethylation (H3K36me1/2) and trimethylation (H3K36me3), respectively, and characterized their roles in the production of antisense transcripts under nutrient‐rich conditions. Using our new bioinformatics identification pipeline analysis, we are able to identify a larger number of antisense transcripts in set2∆ cells than has been published previously. We further show that H3K36me1/2 or H3K36me3 redundantly repressed the production of antisense transcripts. Moreover, gene ontology (GO) analysis implies that H3K36me3‐mediated antisense transcription might play a role in DNA replication and DNA damage repair, which is independent of regulation of the corresponding sense gene expression. Overall, our results validate a coregulatory mechanism of different H3K36 methylation states, particularly in the repression of antisense transcription.https://doi.org/10.1002/2211-5463.13226antisense transcriptionH3K36 methylationSet2
spellingShingle Yu‐Chao Mei
Jiangpeng Feng
Fei He
Yu‐Min Li
Yafei Liu
Feng Li
Yu Chen
Hai‐Ning Du
Set2‐mediated H3K36 methylation states redundantly repress the production of antisense transcripts: role in transcription regulation
FEBS Open Bio
antisense transcription
H3K36 methylation
Set2
title Set2‐mediated H3K36 methylation states redundantly repress the production of antisense transcripts: role in transcription regulation
title_full Set2‐mediated H3K36 methylation states redundantly repress the production of antisense transcripts: role in transcription regulation
title_fullStr Set2‐mediated H3K36 methylation states redundantly repress the production of antisense transcripts: role in transcription regulation
title_full_unstemmed Set2‐mediated H3K36 methylation states redundantly repress the production of antisense transcripts: role in transcription regulation
title_short Set2‐mediated H3K36 methylation states redundantly repress the production of antisense transcripts: role in transcription regulation
title_sort set2 mediated h3k36 methylation states redundantly repress the production of antisense transcripts role in transcription regulation
topic antisense transcription
H3K36 methylation
Set2
url https://doi.org/10.1002/2211-5463.13226
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