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

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

PROVIDER: PRJNA422067 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6367980_1.fastq.gz	Fastqsanger.gz
	SRR6367980_2.fastq.gz	Fastqsanger.gz
	SRR6367990_1.fastq.gz	Fastqsanger.gz
	SRR6367990_2.fastq.gz	Fastqsanger.gz
	SRR6368000_1.fastq.gz	Fastqsanger.gz

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

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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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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.

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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.

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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.

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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:Chromosomal double-strand breaks (DSBs) are resected by 5M-bM-^@M-^Y-nucleases to form 3M-bM-^@M-^Y single-strand DNA (ssDNA) substrates for binding by homologous recombination and DNA damage checkpoint proteins. Two redundant pathways of extensive resection were 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 have identified the yeast nucleosome remodeling enzyme Fun30 as novel factor promoting DSB end resection. Fun30 is the major nucleosome remodeler promoting extensive Exo1- and Sgs1-dependent resection of DSBs while the RSC and INO80 chromatin remodeling complexes play redundant roles with Fun30 in resection adjacent to DSB ends. ATPase and helicase domains of Fun30, which are needed for nucleosome remodeling, are also required for resection. Fun30 is robustly recruited to DNA breaks and spreads around 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 5M-bM-^@M-^Y strand processing and in the absence of either histone H3 K79 methylation or M-NM-3-H2A, which mediate recruitment of the Rad9 . Together these data suggest that Fun30 helps to overcome the inhibitory effect of Rad9 on DNA resection. Genome-wide expression profiling of Yeast gene expression in two cell type including the wild type and a FUN30 knockout cell, each cell type is tested in two duplicates. Test relative gene integration efficiency in yeast genome-wide homozygous diploid deletion mutants.

2012-10-04 | E-GEOD-38601 | biostudies-arrayexpress

The Fun30 ATP-dependent nucleosome remodeler promotes resection of DNA double-strand break ends

Project description:Chromosomal double-strand breaks (DSBs) are resected by 5’-nucleases to form 3’ single-strand DNA (ssDNA) substrates for binding by homologous recombination and DNA damage checkpoint proteins. Two redundant pathways of extensive resection were 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 have identified the yeast nucleosome remodeling enzyme Fun30 as novel factor promoting DSB end resection. Fun30 is the major nucleosome remodeler promoting extensive Exo1- and Sgs1-dependent resection of DSBs while the RSC and INO80 chromatin remodeling complexes play redundant roles with Fun30 in resection adjacent to DSB ends. ATPase and helicase domains of Fun30, which are needed for nucleosome remodeling, are also required for resection. Fun30 is robustly recruited to DNA breaks and spreads around 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 the Rad9 . Together these data suggest that Fun30 helps to overcome the inhibitory effect of Rad9 on DNA resection.

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