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RecG Directs DNA Synthesis During Double-Strand Break Repair [ChIP-seq]

ABSTRACT: In the bacterium Escherichia coli, RecG directs DNA synthesis during the repair of DNA double-strand breaks by homologous recombination.

ORGANISM(S): Escherichia coli

PROVIDER: GSE77181 | GEO | 2016/05/19

SECONDARY ACCESSION(S): PRJNA309668

REPOSITORIES: GEO

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RecG Directs DNA Synthesis During Double-Strand Break Repair [ChIP-seq]

Project description:In the bacterium Escherichia coli, RecG directs DNA synthesis during the repair of DNA double-strand breaks by homologous recombination. Examination of RecA binding during double-strand break repair in Escherichia coli in the presence and absence of RecG protein

2016-05-19 | E-GEOD-77181 | biostudies-arrayexpress

RecG Directs DNA Synthesis During Double-Strand Break Repair [Chromosomal marker frequency analysis]

Project description:In the bacterium Escherichia coli, RecG directs DNA synthesis during the repair of DNA double-strand breaks by homologous recombination.

2016-05-19 | GSE77183 | GEO

RecG Directs DNA Synthesis During Double-Strand Break Repair [Chromosomal marker frequency analysis]

Project description:In the bacterium Escherichia coli, RecG directs DNA synthesis during the repair of DNA double-strand breaks by homologous recombination. Chromosomal marker frequency analysis (MFA) following induction of a DSB in the absence and presence of RecG

2016-05-19 | E-GEOD-77183 | biostudies-arrayexpress

RecG Directs DNA Synthesis During Double-Strand Break Repair

Project description:RecG Directs DNA Synthesis During Double-Strand Break Repair

| PRJNA309667 | ENA

RecG Directs DNA Synthesis during Double-Strand Break Repair.

Project description:Homologous recombination provides a mechanism of DNA double-strand break repair (DSBR) that requires an intact, homologous template for DNA synthesis. When DNA synthesis associated with DSBR is convergent, the broken DNA strands are replaced and repair is accurate. However, if divergent DNA synthesis is established, over-replication of flanking DNA may occur with deleterious consequences. The RecG protein of Escherichia coli is a helicase and translocase that can re-model 3-way and 4-way DNA structures such as replication forks and Holliday junctions. However, the primary role of RecG in live cells has remained elusive. Here we show that, in the absence of RecG, attempted DSBR is accompanied by divergent DNA replication at the site of an induced chromosomal DNA double-strand break. Furthermore, DNA double-stand ends are generated in a recG mutant at sites known to block replication forks. These double-strand ends, also trigger DSBR and the divergent DNA replication characteristic of this mutant, which can explain over-replication of the terminus region of the chromosome. The loss of DNA associated with unwinding joint molecules previously observed in the absence of RuvAB and RecG, is suppressed by a helicase deficient PriA mutation (priA300), arguing that the action of RecG ensures that PriA is bound correctly on D-loops to direct DNA replication rather than to unwind joint molecules. This has led us to put forward a revised model of homologous recombination in which the re-modelling of branched intermediates by RecG plays a fundamental role in directing DNA synthesis and thus maintaining genomic stability.

| S-EPMC4752480 | biostudies-literature

RecG Directs DNA Synthesis During Double-Strand Break Repair

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-05-19 | E-GEOD-77184 | biostudies-arrayexpress

RecG Directs DNA Synthesis During Double-Strand Break Repair

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

2016-05-19 | GSE77184 | GEO

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

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

2018-07-18 | GSE107972 | GEO

CHD7- and HDAC1/2-dependent chromatin remodeling activities cooperate to promote DNA double-strand break repair

Project description:The DNA double-strand break (DSB) response is a multi-step process that requires chromatin reorganization at each stage. 53BP1 is a nodal point in this response as it directs chromatin-based DSB repair. However, how chromatin reorganization impacts DSB repair upstream of 53BP1 is not fully understood. Here we reveal that Chromodomain Helicase DNA Binding Protein 7 (CHD7) rapidly recruits to damaged chromatin in a poly(ADP-ribose) polymerase 1 (PARP1)-dependent manner. CHD7 facilitates chromatin relaxation and the loading of canonical non-homologous end-joining (cNHEJ) factors, while restraining 53BP1 accumulation at DSBs. Moreover, CHD7 physically associates with HDAC1/2, thereby recruiting this complex to DNA breaks independently of its chromatin remodeling activity. HDAC1/2 promote histone H4 de-acetylation and chromatin re-compaction to prevent supraphysiological retention of cNHEJ factors at DBSs. Thus, the cooperation between distinct yet coordinated chromatin remodeling activities driven by CHD7 and HDAC1/2 ensures proper assembly dynamics of the cNHEJ machinery and efficient DSB repair.

2020-08-28 | PXD014339 | Pride

FOXL2 directs DNA double-strand break repair pathways by differentially interacting with Ku.

Project description:The balance between major DNA double-strand break (DSB) repair pathways is influenced by binding of the Ku complex, a XRCC5/6 heterodimer, to DSB ends, initiating non-homologous end joining (NHEJ) but preventing additional DSB end resection and homologous recombination (HR). However, the key molecular cue for Ku recruitment to DSB sites is unknown. Here, we report that FOXL2, a forkhead family transcriptional factor, directs DSB repair pathway choice by acetylation-dependent binding to Ku. Upon DSB induction, SIRT1 translocates to the nucleus and deacetylates FOXL2 at lysine 124, leading to liberation of XRCC5 and XRCC6 from FOXL2 and formation of the Ku complex. FOXL2 ablation enhances Ku recruitment to DSB sites, imbalances DSB repair kinetics by accelerating NHEJ and inhibiting HR, and thus leads to catastrophic genomic events. Our study unveils the SIRT1-(de)acetylated FOXL2-Ku axis that governs the balance of DSB repair pathways to maintain genome integrity.

| S-EPMC7181608 | biostudies-literature

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