Effects of oxidative stress on mitotic recombination and genomic stability in yeast after 20 passages
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ABSTRACT:
PROVIDER: PRJNA419211 | ENA |
REPOSITORIES: ENA
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Project description:Oxidative stress is a common factor threatening genomic stability in almost all aerobic organisms. Using a yeast screening system, we measured the frequency of mitotic recombination was greatly elevated after H2O2 treatment. H2O2 was able to break chromatid directly in G1 synchronized cells and homologous recombination was induced to repair DNA double stand breaks at S/G2 phase. By whole genome SNP microarray and sequencing, the patterns of H2O2 induced loss of heterozygosity (LOH; gene conversion and crossover), chromosomal rearrangement, and aneuploidy changes were revealed. LOH events were the most common genomic alterations induced by H2O2 and were randomly distributed throughout the genome.
2017-11-21 | GSE107178 | GEO
Project description:Oxidative stress is a common factor threating genomic stability in almost all aerobic organisms. Using a yeast screening system, we measured the frequency of mitotic recombination was greatly elevated after H2O2 treatment. H2O2 was able to break chromatid directly in G1 synchronized cells and homologous recombination was induced to repair DNA double stand breaks at S/G2 phase. By whole genome SNP microarray and sequencing, the patterns of H2O2 induced loss of heterozygosity (LOH; gene conversion and crossover), chromosomal rearrangement, and aneuploidy changes were revealed. LOH events were the most common genomic alterations induced by H2O2 and were randomly distributed throughout the genome.
2017-11-15 | GSE106816 | GEO
Project description:Effects of oxidative stress on mitotic recombination and genomic stability in yeast
| PRJNA418280 | ENA
Project description:Homologous recombination is essential for high-fidelity DNA repair during mitotic proliferation and meiosis. Yet, context-specific modifications must tailor the recombination machinery to avoid, or enforce, formation of reciprocal exchanges – crossovers – between recombining chromosomes. To obtain molecular insight into how crossover control is achieved, we affinity-purified the 7 DNA-processing enzymes with known roles in channelling HR intermediates into crossovers, or non-crossovers, from vegetative cells, or cells undergoing meiosis. Using mass spectrometry, we provide the first global characterization of their composition. The resulting mitosis- and meiosis-specific interaction maps reveal intricate changes in enzyme architecture and a concerted rewiring of the interaction networks to support flexible control to the recombination outcome. Moreover, functional analyses of 31 novel interactions uncovered 8 meiosis-specific network components that remodel HR to support crossing-over. Chd1, which transiently associates with Exo1 during meiosis, enables the formation of MutLγ-Exo1-dependent crossovers through its conserved ability to bind and displace nucleosomes.
2019-07-31 | PXD012486 | Pride
Project description:In yeast, DNA breaks are usually repaired by homologous recombination (HR). An early step for HR pathways is formation of a heteroduplex, in which a single-strand from the broken DNA molecule pairs with a strand derived from an intact DNA molecule. If the two strands of DNA are not identical, there will be mismatches within the heteroduplex DNA (hetDNA). In wild-type strains, these mismatches are repaired by the mismatch repair (MMR) system, producing a gene conversion event. In strains lacking MMR, the mismatches persist. Most previous studies involving hetDNA formed during mitotic recombination were restricted to one locus. Below, we present a global mapping of hetDNA formed in the MMR-defective mlh1 strain. We find that many recombination events are associated with repair of double-stranded DNA gaps and/or involve Mlh1-independent mismatch repair. Many of our events are not explicable by the simplest form of the double-strand break repair model of recombination.
2017-06-27 | GSE100497 | GEO
Project description:The Saccharomyces cerevisae RAD3 gene is homolog of human XPD, an essential gene encoding a DNA helicase of the TFIIH complex involved in both nucleotide excision repair (NER) and transcription. Mutant alleles of RAD3 have been identified (rad3-101 and rad3-102) that have partial defects in DNA repair associated with a strong hyper-recombination (hyper-Rec) phenotype. Previous studies showed that the hyper-Rec phenotype associated with rad3-101 and rad3-102 can be explained as a consequence of persistent single-stranded DNA gaps that are converted to recombinogenic double-strand breaks (DSBs) by replication. We have further characterized these events using a system in which the reciprocal products of mitotic recombination between homologs are recovered as red and white sectored colonies. Both rad3-101 and rad3-102 elevate the frequency of sectored colonies about 100-fold. Subsequent mapping of these events shows that three-quarters of crossovers between homologs induced in hyper-Rec rad3 mutants reflect DSBs formed in at the same positions in both sister chromatids (double sister-chromatid breaks, DSCBs). The remainder reflects DSBs formed in single chromatids (single chromatid breaks, SCBs). The ratio of DSCBs to SCBs is similar to that observed for spontaneous recombination events in wild-type cells. In addition to examining crossovers on chromosome V, we mapped 216 unselected genomic alterations throughout the genome including crossovers, gene conversions, deletions, and duplications. We found a significant association between the location of these recombination events and regions with elevated gamma-H2AX. In addition, there was a hotspot for deletions and duplications at the IMA2 and HXT11 genes near the left end of chromosome XV. A comparison of these data with our previous analysis of spontaneous mitotic recombination events suggests that a sub-set of spontaneous events in wild-type cells may be initiated by incomplete NER reactions, and that DSCBs, which cannot be repaired by sister-chromatid recombination, are a major source of mitotic recombination between homologous chromosomes.
2015-12-30 | GSE76395 | GEO
Project description:The histone variant H2A.Z is one of the most evolutionally conserved histone variants. Here, we identified a cancer-associated mutation in H2A.Z and evaluate the mutation. Structural and biochemical in vitro analyses showed that the H2A.Z mutation destabilizes nucleosome containing it. Then we applied the genetic complementation analysis to analyze cellular functions of the H2A.Z mutant. Although the H2A.Z mutant is deposited into nucleosome and rescues the lethality of H2A.Z DKO cells, the mutant does not complement mitotic defects of H2A.Z DKO cells, suggesting that stability of H2A.Z nucleosome is required for proper mitotic progression. Importantly, the H2A.Z mutant led to mitotic defects even in the presence of a larger pool of wild-type H2A.Z. Thus, it is implicated that the cancer-associated mutation appeared in an allele of the H2A.Z isoform genes would be involved in carcinogenesis through causing mitotic defects.
2024-10-28 | GSE84647 | GEO
Project description:Cohesin removal reprograms mitotic gene expression upon mitotic entry
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Project description:We established a large panel of preclinical models of human RCC directly from patients, faithfully reproducing the biological features of the original tumor. RCC tissues were collected for 8 years from 336 patients undergoing surgery, xenografted subcutaneously in nude mice, and serially passaged into new mice up to 13 passages. Tissue samples from the primary tumor and tumors grown in mice through passages were analyzed at the histology, genetic and for of them at the molecular levels for biological tissue stability. We established a large panel of 30 RCC models and 5 them of the clear cell type (clear cell renal cell carcinoma, CCC) were characterized at the mRNA expression level.
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