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Disabling leading and lagging strand histone transmission results in parental histones loss and reduced cell plasticity and viability [SCAR-seq]

ABSTRACT: Disabling leading and lagging strand histone transmission results in parental histones loss and reduced cell plasticity and viability [SCAR-seq]

PROVIDER: PRJNA1126116 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29471749.fastq.gz	Fastqsanger.gz
	SRR29471750.fastq.gz	Fastqsanger.gz
	SRR29471751.fastq.gz	Fastqsanger.gz
	SRR29471752.fastq.gz	Fastqsanger.gz
	SRR29471753.fastq.gz	Fastqsanger.gz

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Disabling leading and lagging strand histone transmission results in parental histones loss and reduced cell plasticity and viability [SCAR-seq]

Project description:In the process of DNA replication, the first steps in restoring the chromatin landscape involve parental histone recycling and new histone deposition. Disrupting histone recycling to either the leading or lagging strand induces asymmetric histone inheritance, impacting epigenome maintenance and cellular identity. However, the order and kinetics of these effects remain elusive. Here, we employ inducible mutants to dissect the early and late consequences of impaired histone recycling. Simultaneous disruption of both leading (POLE4) and lagging strand (MCM2-2A) recycling pathways impairs transmission of parental histones to newly synthesized DNA, with release of some parental histones to the soluble pool. Subsequently, H3K27me3 accumulates aberrantly during chromatin restoration in a manner preceding gene expression changes. Loss of histone inheritance and the ensuing chromatin restoration defects alter gene expression in embryonic stem cells, challenges differentiation programs and cell viability. Our findings demonstrate the importance of efficient transmission of histone-based information during DNA replication for maintaining chromatin landscapes, differentiation potential, and cellular viability.

2025-01-10 | GSE270279 | GEO

Disabling leading and lagging strand histone transmission results in parental histones loss and reduced cell plasticity and viability [RNA-Seq]

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Disabling leading and lagging strand histone transmission results in parental histones loss and reduced cell plasticity and viability [repliATAC-seq]

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Disabling leading and lagging strand histone transmission results in parental histones loss and reduced cell plasticity and viability [ChOR-seq]

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Disabling leading and lagging strand histone transmission results in parental histones loss and reduced cell plasticity and viability

Project description:Disabling leading and lagging strand histone transmission results in parental histones loss and reduced cell plasticity and viability

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Disabling leading and lagging strand histone transmission results in parental histones loss and reduced cell plasticity and viability [repliATAC-seq]

Project description:Disabling leading and lagging strand histone transmission results in parental histones loss and reduced cell plasticity and viability [repliATAC-seq]

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Disabling leading and lagging strand histone transmission results in parental histones loss and reduced cell plasticity and viability [RNA-Seq]

Project description:Disabling leading and lagging strand histone transmission results in parental histones loss and reduced cell plasticity and viability [RNA-Seq]

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Disabling leading and lagging strand histone transmission results in parental histones loss and reduced cell plasticity and viability [ChOR-seq]

Project description:Disabling leading and lagging strand histone transmission results in parental histones loss and reduced cell plasticity and viability [ChOR-seq]

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The fork protection complex promotes symmetric histone recycling to maintain heterochromatin [SCAR-seq]

Project description:The inheritance of parental histones across the replication fork is thought to mediate epigenetic memory. Here, we reveal that fission yeast Mrc1 (Claspin in humans) binds H3-H4 tetramers and operates as a central coordinator of symmetric parental histone inheritance. Mrc1 mutants in a key connector domain disrupted segregation of parental histones to the lagging strand comparable to Mcm2 histone-binding mutants. Both mutants showed clonal and asymmetric loss of H3K9me-mediated gene silencing. AlphaFold predicted co-chaperoning of H3-H4 tetramers by Mrc1 and Mcm2, with the Mrc1 connector domain bridging histone and Mcm2 binding. Biochemical and functional analysis validated this model and revealed a duality in Mrc1 function: disabling histone binding in the connector domain disrupted lagging strand recycling while another histone-binding mutation impaired leading strand recycling. We propose Mrc1 toggles histones between the lagging and leading strand recycling pathways, in part by intra-replisome co-chaperoning, to ensure epigenetic transmission to both daughter cells.

2024-08-01 | GSE241062 | GEO