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RIF1 regulates replication origin activity and early replication timing in B cells [ChIP-seq]

ABSTRACT: RIF1 regulates replication origin activity and early replication timing in B cells [ChIP-seq]

PROVIDER: PRJNA951770 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24055118.fastq.gz	Fastqsanger.gz
	SRR24055119.fastq.gz	Fastqsanger.gz
	SRR24055120.fastq.gz	Fastqsanger.gz
	SRR24055121.fastq.gz	Fastqsanger.gz

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RIF1 regulates replication origin activity and early replication timing in B cells [PRO-seq]

Project description:The mammalian DNA replication timing (RT) program is crucial for the proper functioning and integrity of the genome. The best-known mechanism for controlling RT is the suppression of late origins of replication in heterochromatin by RIF1. Here, we report that in antigen-activated, hypermutating B lymphocytes, RIF1 binds predominantly to early-replicating active chromatin, regulates early origin firing and promotes early replication. However, RIF1 has a minor role in gene expression and genome organization in B cells. Furthermore, we find that RIF1 functions in a complementary and non-epistatic manner with minichromosome maintenance (MCM) proteins to establish early RT signatures genome-wide and, specifically, to ensure the early replication of highly transcribed genes. These findings reveal a new layer of regulation within the B cell RT program, driven by the coordinated activity of RIF1 and MCM proteins.

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