Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1121202 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29317200_1.fastq.gz | Fastqsanger.gz | |||
| SRR29317200_2.fastq.gz | Fastqsanger.gz | |||
| SRR29317201_1.fastq.gz | Fastqsanger.gz | |||
| SRR29317201_2.fastq.gz | Fastqsanger.gz | |||
| SRR29317202_1.fastq.gz | Fastqsanger.gz |
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Project description:The histone H3.1 variant is specifically inserted on chromatin during DNA replication in eukaryotes. A single amino acid variation (position 31) in the N-terminal tail of H3.1 compared to replication-independent H3.3 is conserved in plants and animals, but no function has been assigned to amino acid 31 to justify a role for H3.1 during replication. In this study, we demonstrate that the protein TONSOKU (TSK/TONSL), which participates in rescuing broken replication forks, specifically interacts with H3.1 via recognition of alanine 31 by its tetratricopeptide repeat (TPR) domain. We show that genomic amplification in the absence of H3K27me1 in plants depends on H3.1, TSK and DNA polymerase theta (Pol θ). Overall, our study reveals similar strategies in plants and animals for regulating TSK activity and post-replicative chromatin maturation, with both clades using the H3.1 variant and different histone mono-methyltransferases (ATXR5/ATXR6 or SET8) to achieve this.
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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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