Genomics

Dataset Information

99

Rec114 ChIP-seq


ABSTRACT: DNA duplication is intimately connected to setting up post-replicative chromosome structures and events, but molecular details of this coordination are not well understood. A striking example occurs during yeast meiosis, where replication locally influences timing of the DNA double-strand breaks (DSBs) that initiate recombination. We show here that replication-DSB coordination is eliminated by overexpressing Dbf4-dependent Cdc7 kinase (DDK) or removing Tof1 or Csm3, components of the replication fork protection complex (FPC). DDK physically associates with Tof1, and Tof1 is dispensable for replication-DSB coordination if DDK is artificially tethered to replisomes. Furthermore, DDK phosphorylation of the DSB-promoting factor Mer2 is locally coordinated with replication, dependent on Tof1. These findings indicate that DDK recruited by FPC to replisomes phosphorylates chromatin-bound Mer2 in the wake of the replication fork, thus synchronizing replication with an early prerequisite for DSB formation. This may be a general mechanism to ensure spatial and temporal coordination of replication with other chromosomal processes. Ninety-six samples total: 12 time points (each time points contains ChIP and input samples) from Rec114-myc ARS+, Rec114-myc ars∆ strains, Rec114-myc tof1∆ARS+ and Rec114-myc tof1∆ ars∆ strains

ORGANISM(S): Saccharomyces cerevisiae  

SUBMITTER: Hajime Murakami  Bic MSKCC   Scott Keeney    

PROVIDER: E-GEOD-52970 | ArrayExpress | 2014-09-06

SECONDARY ACCESSION(S): SRP033495GSE52970PRJNA230576

REPOSITORIES: GEO, ArrayExpress, ENA

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