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

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

ORGANISM(S): Escherichia coli K-12

PROVIDER: GSE107974 | 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.

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.

| S-EPMC6061781 | biostudies-literature

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 [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

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

| PRJNA422067 | ENA

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]

| PRJNA422161 | ENA

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]

| PRJNA422162 | ENA

p73 coordinates with ?133p53 to promote DNA double-strand break repair.

Project description:Tumour repressor p53 isoform ?133p53 is a target gene of p53 and an antagonist of p53-mediated apoptotic activity. We recently demonstrated that ?133p53 promotes DNA double-strand break (DSB) repair by upregulating transcription of the repair genes RAD51, LIG4 and RAD52 in a p53-independent manner. However, ?133p53 lacks the transactivation domain of full-length p53, and the mechanism by which it exerts transcriptional activity independently of full-length p53 remains unclear. In this report, we describe the accumulation of high levels of both ?133p53 and p73 (a p53 family member) at 24?h post ?-irradiation (hpi). ?133p53 can form a complex with p73 upon ?-irradiation. The co-expression of ?133p53 and p73, but not either protein alone, can significantly promote DNA DSB repair mechanisms, including homologous recombination (HR), non-homologous end joining (NHEJ) and single-strand annealing (SSA). p73 and ?133p53 act synergistically to promote the expression of RAD51, LIG4 and RAD52 by joining together to bind to region containing a ?133p53-responsive element (RE) and a p73-RE in the promoters of all three repair genes. In addition to its accumulation at 24?hpi, p73 protein expression also peaks at 4?hpi. The depletion of p73 not only reduces early-stage apoptotic frequency (4-6?hpi), but also significantly increases later-stage DNA DSB accumulation (48?hpi), leading to cell cycle arrest in the G2 phase and, ultimately, cell senescence. In summary, the apoptotic regulator p73 also coordinates with ?133p53 to promote DNA DSB repair, and the loss of function of p73 in DNA DSB repair may underlie spontaneous and carcinogen-induced tumorigenesis in p73 knockout mice.

| S-EPMC5988805 | biostudies-other

A histone H3K36 chromatin switch coordinates DNA double-strand break repair pathway choice.

Project description:DNA double-strand break (DSB) repair is a highly regulated process performed predominantly by non-homologous end joining (NHEJ) or homologous recombination (HR) pathways. How these pathways are coordinated in the context of chromatin is unclear. Here we uncover a role for histone H3K36 modification in regulating DSB repair pathway choice in fission yeast. We find Set2-dependent H3K36 methylation reduces chromatin accessibility, reduces resection and promotes NHEJ, while antagonistic Gcn5-dependent H3K36 acetylation increases chromatin accessibility, increases resection and promotes HR. Accordingly, loss of Set2 increases H3K36Ac, chromatin accessibility and resection, while Gcn5 loss results in the opposite phenotypes following DSB induction. Further, H3K36 modification is cell cycle regulated with Set2-dependent H3K36 methylation peaking in G1 when NHEJ occurs, while Gcn5-dependent H3K36 acetylation peaks in S/G2 when HR prevails. These findings support an H3K36 chromatin switch in regulating DSB repair pathway choice.

| S-EPMC4535359 | biostudies-literature

Tetrameric Ctp1 coordinates DNA binding and DNA bridging in DNA double-strand-break repair.

Project description:Ctp1 (also known as CtIP or Sae2) collaborates with Mre11-Rad50-Nbs1 to initiate repair of DNA double-strand breaks (DSBs), but its functions remain enigmatic. We report that tetrameric Schizosaccharomyces pombe Ctp1 contains multivalent DNA-binding and DNA-bridging activities. Through structural and biophysical analyses of the Ctp1 tetramer, we define the salient features of Ctp1 architecture: an N-terminal interlocking tetrameric helical dimer-of-dimers (THDD) domain and a central intrinsically disordered region (IDR) linked to C-terminal 'RHR' DNA-interaction motifs. The THDD, IDR and RHR are required for Ctp1 DNA-bridging activity in vitro, and both the THDD and RHR are required for efficient DSB repair in S. pombe. Our results establish non-nucleolytic roles of Ctp1 in binding and coordination of DSB-repair intermediates and suggest that ablation of human CtIP DNA binding by truncating mutations underlie the CtIP-linked Seckel and Jawad syndromes.

| S-EPMC4318798 | biostudies-literature

Quantitative genomic analysis of RecA protein binding during DNA double-strand break repair reveals RecBCD action in vivo.

Project description:Understanding molecular mechanisms in the context of living cells requires the development of new methods of in vivo biochemical analysis to complement established in vitro biochemistry. A critically important molecular mechanism is genetic recombination, required for the beneficial reassortment of genetic information and for DNA double-strand break repair (DSBR). Central to recombination is the RecA (Rad51) protein that assembles into a spiral filament on DNA and mediates genetic exchange. 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. We have used quantitative genomic analysis to infer the key in vivo molecular parameters governing RecA loading by the helicase/nuclease RecBCD at recombination hot-spots, known as Chi. Our genomic analysis has also revealed that DSBR at the lacZ locus causes a second RecBCD-mediated DSBR event to occur in the terminus region of the chromosome, over 1 Mb away.

| S-EPMC4553759 | biostudies-literature

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