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

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

PROVIDER: PRJNA1126146 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29452400_1.fastq.gz	Fastqsanger.gz
	SRR29452400_2.fastq.gz	Fastqsanger.gz
	SRR29471900.fastq.gz	Fastqsanger.gz
	SRR29452401_1.fastq.gz	Fastqsanger.gz
	SRR29452401_2.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.

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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 [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 [SCAR-seq]

Project description:Disabling leading and lagging strand histone transmission results in parental histones loss and reduced cell plasticity and viability [SCAR-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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CAF-1 deposits newly synthesized histones during DNA replication using distinct mechanisms on the leading and lagging strands

Project description:During every cell cycle, both the genome and the associated chromatin must be accurately replicated. Chromatin Assembly Factor-1 (CAF-1) is a key regulator of chromatin replication, but how CAF-1 functions in relation to the DNA replication machinery is unknown. Here, we reveal that this crosstalk differs between the leading and lagging strand at replication forks. Using biochemical reconstitution, we show that DNA and histones promote CAF-1 recruitment to its binding partner PCNA and reveal that two CAF-1 complexes are required for efficient nucleosome assembly under these conditions. Remarkably, in the context of the replisome, CAF-1 competes with the leading strand DNA polymerase epsilon (Pole) for PCNA binding. However, CAF-1 does not affect the activity of the lagging strand DNA polymerase Delta (Pold). Yet, in cells, CAF-1 deposits newly synthesized histones equally on both daughter strands. Thus, on the leading strand, chromatin assembly by CAF-1 cannot occur simultaneously to DNA synthesis, while on the lagging strand these processes may be coupled. We propose that these differences may facilitate distinct parental histone recycling mechanisms and accommodate the inherent asymmetry of DNA replication.

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