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TONSOKU is required for the maintenance of repressive epigenetic modifications in Arabidopsis [MNase-seq]

ABSTRACT: Epigenetic inheritance requires the faithful maintenance of epigenetic marks such as certain chromatin modifications through DNA replication. Plant TONSOKU (TSK) and its animal orthologue TONSOKU-like (TONSL) act as readers for newly synthesized histones and assist in DNA replication via facilitating DNA damage repair at post-replicative chromatin. However, whether TSK/TONSL regulates chromatin replication and the maintenance of chromatin modifications remain elusive. In this study, we demonstrate that TSK is dispensable for global histone and nucleosome accumulation but necessary for maintaining repressive chromatin modifications including H3K9me2, H2A.W, H3K27me3 and DNA methylation. TSK physically interacts with H3K9 methyltransferases SUVH5 and SUVH6, and the Polycomb protein RING1a/b. Moreover, TSK mutation strongly enhances defects in Polycomb pathway mutants. TSK is intended to only associate with nascent chromatin until it starts to mature. We propose that TSK ensures proper epigenetic inheritance by supporting the recruitment of epigenetic modifiers to post-replicative chromatin in a critical short window of time following DNA replication.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE229474 | GEO | 2023/06/08

REPOSITORIES: GEO

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TONSOKU is required for the maintenance of repressive epigenetic modifications in Arabidopsis [RNA-Seq]

Project description:Epigenetic inheritance requires the faithful maintenance of epigenetic marks such as certain chromatin modifications through DNA replication. Plant TONSOKU (TSK) and its animal orthologue TONSOKU-like (TONSL) act as readers for newly synthesized histones and assist in DNA replication via facilitating DNA damage repair at post-replicative chromatin. However, whether TSK/TONSL regulates chromatin replication and the maintenance of chromatin modifications remain elusive. In this study, we demonstrate that TSK is dispensable for global histone and nucleosome accumulation but necessary for maintaining repressive chromatin modifications including H3K9me2, H2A.W, H3K27me3 and DNA methylation. TSK physically interacts with H3K9 methyltransferases SUVH5 and SUVH6, and the Polycomb protein RING1a/b. Moreover, TSK mutation strongly enhances defects in Polycomb pathway mutants. TSK is intended to only associate with nascent chromatin until it starts to mature. We propose that TSK ensures proper epigenetic inheritance by supporting the recruitment of epigenetic modifiers to post-replicative chromatin in a critical short window of time following DNA replication.

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