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RecBCD Coordinates Repair of Two Ends at a DNA Double-Strand Break, Preventing Aberrant Chromosome Amplification [ChIP-seq]

ABSTRACT: In the bacterium Escherichia coli, RecBCD coordinates repair of two ends at a DNA double-strand break, preventing aberrant chromosome amplification

ORGANISM(S): Escherichia coli K-12

PROVIDER: GSE107972 | GEO | 2018/07/18

REPOSITORIES: GEO

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RecBCD Coordinates Repair of Two Ends at a DNA Double-Strand Break, Preventing Aberrant Chromosome Amplification [MFA]

Project description:The effect of an induced site-specific DNA double-strand break on DNA abundance across the chromosome of E. coli cells expressing or not RecD protein, was investigated by marker frequency analysis.

2018-07-18 | GSE107973 | GEO

RecBCD coordinates repair of two ends at a DNA double-strand break, preventing aberrant chromosome amplification.

Project description:DNA double-strand break (DSB) repair is critical for cell survival. A diverse range of organisms from bacteria to humans rely on homologous recombination for accurate DSB repair. This requires both coordinate action of the two ends of a DSB and stringent control of the resultant DNA replication to prevent unwarranted DNA amplification and aneuploidy. In Escherichia coli, RecBCD enzyme is responsible for the initial steps of homologous recombination. Previous work has revealed recD mutants to be nuclease defective but recombination proficient. Despite this proficiency, we show here that a recD null mutant is defective for the repair of a two-ended DSB and that this defect is associated with unregulated chromosome amplification and defective chromosome segregation. Our results demonstrate that RecBCD plays an important role in avoiding this amplification by coordinating the two recombining ends in a manner that prevents divergent replication forks progressing away from the DSB site.

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RecBCD Coordinates Repair of Two Ends at a DNA Double-Strand Break, Preventing Aberrant Chromosome Amplification

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-07-18 | GSE107974 | GEO

RecBCD Coordinates Repair of Two Ends at a DNA Double-Strand Break, Preventing Aberrant Chromosome Amplification

Project description:RecBCD Coordinates Repair of Two Ends at a DNA Double-Strand Break, Preventing Aberrant Chromosome Amplification

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RecBCD Coordinates Repair of Two Ends at a DNA Double-Strand Break, Preventing Aberrant Chromosome Amplification [MFA]

Project description:RecBCD Coordinates Repair of Two Ends at a DNA Double-Strand Break, Preventing Aberrant Chromosome Amplification [MFA]

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RecBCD Coordinates Repair of Two Ends at a DNA Double-Strand Break, Preventing Aberrant Chromosome Amplification [ChIP-seq]

Project description:RecBCD Coordinates Repair of Two Ends at a DNA Double-Strand Break, Preventing Aberrant Chromosome Amplification [ChIP-seq]

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Quantitative Genomic Analysis of RecA Protein Binding During DNA Double-Strand Break Repair Reveals RecBCD Action in vivo

Project description:Here we have developed a method that combines chromatin immunoprecipitation with next-generation sequencing (ChIP-Seq) and mathematical modeling to quantify RecA protein binding during the active repair of a single DSB in the chromosome of Escherichia coli. Examination of RecA binding during double-strand break repair in Escherichia coli

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Rad52 Restrains Resection at DNA Double-Strand Break Ends in Yeast.

Project description:Rad52 is a key factor for homologous recombination (HR) in yeast. Rad52 helps assemble Rad51-ssDNA nucleoprotein filaments that catalyze DNA strand exchange, and it mediates single-strand DNA annealing. We find that Rad52 has an even earlier function in HR in restricting DNA double-stranded break ends resection that generates 3' single-stranded DNA (ssDNA) tails. In fission yeast, Exo1 is the primary resection nuclease, with the helicase Rqh1 playing a minor role. We demonstrate that the choice of two extensive resection pathways is regulated by Rad52. In rad52 cells, the resection rate increases from ∼3-5 kb/h up to ∼10-20 kb/h in an Rqh1-dependent manner, while Exo1 becomes dispensable. Budding yeast Rad52 similarly inhibits Sgs1-dependent resection. Single-molecule analysis with purified budding yeast proteins shows that Rad52 competes with Sgs1 for DNA end binding and inhibits Sgs1 translocation along DNA. These results identify a role for Rad52 in limiting ssDNA generated by end resection.

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Project description:We used ChIP-seq to assess where p53 binds in the human genome and how that binding changes during the DNA double-strand break response. In particular, we considered the 1-Mb-wide window centered on the MYC locus. Contrary to previous reports, we found no evidence of p53 binding at the MYC promoter. Rather, we identified three locations downstream of MYC at which p53 was bound; binding at each of these regions increased during the DNA double-strand break response.

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The Fun30 nucleosome remodeller promotes resection of DNA double-strand break ends.

Project description:Chromosomal double-strand breaks (DSBs) are resected by 5' nucleases to form 3' single-stranded DNA substrates for binding by homologous recombination and DNA damage checkpoint proteins. Two redundant pathways of extensive resection have been described both in cells and in vitro, one relying on Exo1 exonuclease and the other on Sgs1 helicase and Dna2 nuclease. However, it remains unknown how resection proceeds within the context of chromatin, where histones and histone-bound proteins represent barriers for resection enzymes. Here we identify the yeast nucleosome-remodelling enzyme Fun30 as a factor promoting DSB end resection. Fun30 is the major nucleosome remodeller promoting extensive Exo1- and Sgs1-dependent resection of DSBs. The RSC and INO80 chromatin-remodelling complexes and Fun30 have redundant roles in resection adjacent to DSB ends. ATPase and helicase domains of Fun30, which are needed for nucleosome remodelling, are also required for resection. Fun30 is robustly recruited to DNA breaks and spreads along the DSB coincident with resection. Fun30 becomes less important for resection in the absence of the histone-bound Rad9 checkpoint adaptor protein known to block 5' strand processing and in the absence of either histone H3 K79 methylation or γ-H2A, which mediate recruitment of Rad9 (refs 9, 10). Together these data suggest that Fun30 helps to overcome the inhibitory effect of Rad9 on DNA resection.

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