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RecG Directs DNA Synthesis During Double-Strand Break Repair

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Escherichia coli

PROVIDER: GSE77184 | GEO | 2016/05/19

SECONDARY ACCESSION(S): PRJNA309667

REPOSITORIES: GEO

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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: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 [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 [ChIP-seq]

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 | GSE77181 | 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 [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

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

RAD18 directs DNA double-strand break repair by homologous recombination to post-replicative chromatin.

Project description:RAD18 is an E3 ubiquitin ligase that prevents replication fork collapse by promoting DNA translesion synthesis and template switching. Besides this classical role, RAD18 has been implicated in homologous recombination; however, this function is incompletely understood. Here, we show that RAD18 is recruited to DNA lesions by monoubiquitination of histone H2A at K15 and counteracts accumulation of 53BP1. Super-resolution microscopy revealed that RAD18 localizes to the proximity of DNA double strand breaks and limits the distribution of 53BP1 to the peripheral chromatin nanodomains. Whereas auto-ubiquitination of RAD18 mediated by RAD6 inhibits its recruitment to DNA breaks, interaction with SLF1 promotes RAD18 accumulation at DNA breaks in the post-replicative chromatin by recognition of histone H4K20me0. Surprisingly, suppression of 53BP1 function by RAD18 is not involved in homologous recombination and rather leads to reduction of non-homologous end joining. Instead, we provide evidence that RAD18 promotes HR repair by recruiting the SMC5/6 complex to DNA breaks. Finally, we identified several new loss-of-function mutations in RAD18 in cancer patients suggesting that RAD18 could be involved in cancer development.

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The Dystonia Gene THAP1 Controls DNA Double Strand Break Repair Choice

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

2021-04-13 | GSE154729 | GEO