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

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

PROVIDER: PRJNA1006322 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25663222_1.fastq.gz	Fastqsanger.gz
	SRR25663222_2.fastq.gz	Fastqsanger.gz
	SRR25663223_1.fastq.gz	Fastqsanger.gz
	SRR25663223_2.fastq.gz	Fastqsanger.gz
	SRR25663224_1.fastq.gz	Fastqsanger.gz

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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.

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The fork protection complex promotes symmetric histone recycling to maintain heterochromatin

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The fork protection complex promotes symmetric histone recycling to maintain heterochromatin [ChIP-Seq]

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DONSON encodes a novel replication fork protection factor mutated in 2 microcephalic dwarfism.

Project description:To ensure efficient genome duplication, cells have evolved a multitude of factors that promote unperturbed DNA replication, and protect, repair and restart damaged forks. Here we identify DONSON as a novel fork protection factor, and report biallelic DONSON mutations in individuals with microcephalic dwarfism. We demonstrate that DONSON is a component of the replisome that stabilises forks during normal genome replication. Loss of DONSON leads to severe replication-associated DNA damage arising from nucleolytic cleavage of stalled replication forks. Furthermore, ATR-dependent ,signalling in response to replication stress is impaired in DONSON-deficient cells, resulting in decreased checkpoint activity, and potentiating chromosomal instability. Hypomorphic mutations substantially reduce DONSON protein levels and impair fork stability in patient cells, consistent with defective DNA replication underlying the disease phenotype In summary, we identify mutations in DONSON as a common cause of microcephalic dwarfism, and establish DONSON as a critical replication fork protein required for mammalian DNA replication and genome stability

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Symmetric inheritance of parental histones governs epigenome maintenance and stem cell identity [SCAR-seq]

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DONSON encodes a novel replication fork protection factor mutated in microcephalic dwarfism.

Project description:To ensure efficient genome duplication, cells have evolved a multitude of factors that promote unperturbed DNA replication, and protect, repair and restart damaged forks. Here we identify DONSON as a novel fork protection factor, and report biallelic DONSON mutations in 29 individuals with microcephalic dwarfism. We demonstrate that DONSON is a component of the replisome that stabilises forks during normal genome replication. Loss of DONSON leads to severe replication-associated DNA damage arising from nucleolytic cleavage of stalled replication forks. Furthermore, ATR-dependent signalling in response to replication stress is impaired in DONSON-deficient cells, resulting in decreased checkpoint activity, and potentiating chromosomal instability. Hypomorphic mutations substantially reduce DONSON protein levels and impair fork stability in patient cells, consistent with defective DNA replication underlying the disease phenotype. In summary, we identify mutations in DONSON as a common cause of microcephalic dwarfism, and establish DONSON as a critical replication fork protein required for mammalian DNA replication and genome stability.

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DONSON encodes a novel replication fork protection factor mutated in 2 microcephalic dwarfism.

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