Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

TONSOKU reads the histone H3.1 variant to mediate DNA repair during replication

ABSTRACT: 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.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE184738 | GEO | 2022/12/07

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

TONSOKU is required for the maintenance of repressive epigenetic modifications in Arabidopsis [ChIPSeq-H3K27me3]

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.

2023-06-08 | GSE233961 | GEO

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

2023-06-08 | GSE229477 | GEO

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

2023-06-08 | GSE229474 | GEO

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

2023-06-08 | GSE229466 | GEO

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

2023-06-08 | GSE229461 | GEO

TONSOKU reads the histone H3.1 variant to mediate DNA repair during replication

Project description:TONSOKU reads the histone H3.1 variant to mediate DNA repair during replication

| PRJNA766035 | ENA

DNA replication-coupled histone modification maintains Polycomb gene silencing in plants [ChIP-Rx]

Project description:Propagation of patterns of gene expression through the cell cycle requires prompt restoration of epigenetic marks after the twofold dilution caused by DNA replication. Here, we show that the transcriptional repressive mark histone H3K27 trimethylation (H3K27me3) is restored in replicating plant cells through DNA replication-coupled modification of histone variant H3.1. Plants evolved a mechanism for efficient K27 trimethylation on H3.1, which is essential for inheritance of the silencing memory from mother to daughter cells. We illustrate how this mechanism establishes H3K27me3 mediated silencing during the developmental transition to flowering. Our study reveals transmission of H3K27me3 in plant cells through cell divisions, enabling H3K27me3 to function as an epigenetic mark.

2017-08-20 | GSE101220 | GEO

DNA replication-coupled histone modification maintains Polycomb gene silencing in plants [RNA-seq]

2017-08-20 | GSE101219 | GEO

H3.1K27me1 maintains transcriptional silencing and genome stability by preventing GCN5-mediated histone acetylation

Project description:In plants, genome stability is maintained during DNA replication by the H3K27 methyltransferases ATXR5 and ATXR6, which catalyze the deposition of H3K27me1 on the replication-dependent H3.1 variant. Loss of H3.1K27me1 in atxr5 atxr6 mutants leads to heterochromatin defects, including transcriptional de-repression and genomic instability, but the molecular mechanisms involved remain largely unknown. In this study, we identified the conserved histone acetyltransferase GCN5 as a mediator of transcriptional de-repression and genomic instability in the absence of H3.1K27me1. GCN5 is part of a SAGA-like complex in plants and requires ADA2b and CHR6 to mediate the heterochromatic defects of atxr5 atxr6 mutants. Our results show that GCN5 acetylates multiple lysine residues on H3.1 variants, but that H3.1K27 and H3.1K36 play key roles in inducing genomic instability in the absence of H3.1K27me1. Overall, this work reveals a key molecular role for H3.1K27me1 in maintaining genome stability by preventing GCN5-dependent histone acetylation in plants.

2021-06-04 | GSE146126 | GEO

Quantitative middle-down MS analysis of histone H3 proteoforms throughout lifespan in mice

Project description:Replication-independent deposition of histone variant H3.3 into chromatin is essential for many biological processes, including development, oogenesis and nuclear reprogramming. Unlike replication-dependent H3.1/2 isoforms, H3.3 is expressed throughout the cell cycle and becomes enriched in postmitotic cells with age. However, lifelong dynamics of H3 variant replacement and the impact of this process on chromatin organization remain largely undefined. To address this, we investigated genome-wide changes in histone H3 variants composition and H3 modification abundances throughout the lifespan in mice using quantitative mass spectrometry (MS) – based middle-down proteomics strategy. Using middle-down MS we demonstrate that H3.3 accumulates in the chromatin of various somatic mouse tissues throughout life, resulting in near complete replacement of H3.1/2 isoforms by the late adulthood. Accumulation of H3.3 is associated with profound changes in the global level of H3 methylation. H3.3-containing chromatin exhibits distinct stable levels of H3R17me2 and H3K36me2, different from those on H3.1/H3.2-containing chromatin, indicating a direct link between H3 variant exchange and histone methylation dynamics with age. In summary, our study provides the first time comprehensive characterization of dynamic changes in the H3 modification landscape during mouse lifespan and links these changes to the age-dependent accumulation of histone variant H3.3.

2017-07-28 | PXD005300 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data