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Schizosaccharomyces pombe

ABSTRACT: Histone H3G34R mutation causes replicative stress, defective homologous recombination and genomic instability in Fission Yeast

PROVIDER: PRJNA379911 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5363230_1.fastq.gz	Fastqsanger.gz
	SRR5363230_2.fastq.gz	Fastqsanger.gz
	SRR5363231_1.fastq.gz	Fastqsanger.gz
	SRR5363231_2.fastq.gz	Fastqsanger.gz
	SRR5363232_1.fastq.gz	Fastqsanger.gz

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Project description:Swi1/Timeless prevents repeat instability at fission yeast telomeres

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Histone H3-G34V and H3-G34R mutant fission yeast exhibit distinct chromatin changes and different DNA damage sensitivities.

Project description:Recurrent somatic mutations of H3F3A in aggressive pediatric high-grade gliomas generate K27M or G34R mutant histone H3.3. H3.3-G34R mutants are common in tumors additionally mutant for p53 and ATRX, an H3.3-specific chromatin remodeler. To gain insight into the role of H3-G34R, we generated fission yeast that express only the mutant histone H3. H3-G34R specifically reduces H3K36 tri-methylation and H3K36 acetylation, but minimally affects transcriptional control. H3-G34R mutants exhibit genomic instability and increased replicative stress including slowed replication fork restart although DNA replication checkpoints are functional. H3-G34R mutants are defective for DNA damage repair by homologous recombination (HR), and on damage have altered HR protein dynamics suggestive that H3-G34R slows resolution of HR-mediated repair. In summary our analysis of H3-G34R mutant fission yeast provides mechanistic insight into how G34R mutation may promote genomic instability in glioma.

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Histone H3G34R mutation causes replicative stress, defective homologous recombination and genomic instability in Fission Yeast

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Mapping of Rec12 oligonucleotides in Schizosaccharomyces pombe

Project description:Meiotic recombination facilitates accurate pairing and faithful segregation of homologous chromosomes by forming physical connections (crossovers) between homologs. Developmentally programmed DNA double-strand breaks (DSBs) generated by Spo11 protein (Rec12 in fission yeast) initiate meiotic recombination. Until recently, attempts to address the basis of the highly non-random distribution of DSBs on a genome-wide scale have been limited to 0.1–1 kb resolution of DSB position. We have assessed individual DSB events across the Schizosaccharomyces pombe genome at near-nucleotide resolution by deep-sequencing the short oligonucleotides connected to Rec12 following DNA cleavage. The single oligonucleotide size-class generated by Rec12 allowed us to effectively analyze all break events. Our high-resolution DSB map shows that the influence of underlying nucleotide sequence and chromosomal architecture differs in multiple ways from that in budding yeast. Rec12 action is not strongly restricted to nucleosome-depleted regions but is nevertheless spatially biased with respect to chromatin structure. Furthermore, we find strong evidence across the genome for differential DSB repair previously predicted to account for crossover invariance (constant cM/kb in spite of DSB hotspots). Our genome-wide analyses demonstrate evolutionarily fluid factors contributing to crossover initiation and its regulation.

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Project description:Nucleosomal organization of replication origins and meiotic recombination hotspots in fission yeast

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Schizosaccharomyces pombe

Project description:Histone H3 lysine9 acetylation, rather than lysine4 trimethylation, marks meiotic recombination hotspots and promotes recombination initiation in fission yeast

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Mapping of Rec12 oligonucleotides in Schizosaccharomyces pombe

Project description:Meiotic recombination facilitates accurate pairing and faithful segregation of homologous chromosomes by forming physical connections (crossovers) between homologs. Developmentally programmed DNA double-strand breaks (DSBs) generated by Spo11 protein (Rec12 in fission yeast) initiate meiotic recombination. Until recently, attempts to address the basis of the highly non-random distribution of DSBs on a genome-wide scale have been limited to 0.1M-bM-^@M-^S1 kb resolution of DSB position. We have assessed individual DSB events across the Schizosaccharomyces pombe genome at near-nucleotide resolution by deep-sequencing the short oligonucleotides connected to Rec12 following DNA cleavage. The single oligonucleotide size-class generated by Rec12 allowed us to effectively analyze all break events. Our high-resolution DSB map shows that the influence of underlying nucleotide sequence and chromosomal architecture differs in multiple ways from that in budding yeast. Rec12 action is not strongly restricted to nucleosome-depleted regions but is nevertheless spatially biased with respect to chromatin structure. Furthermore, we find strong evidence across the genome for differential DSB repair previously predicted to account for crossover invariance (constant cM/kb in spite of DSB hotspots). Our genome-wide analyses demonstrate evolutionarily fluid factors contributing to crossover initiation and its regulation. Three samples total: one sample sequenced by 454 and two technical replicates (independent adaptor ligations from material purified from one culture) sequenced by SOLiD

2013-08-20 | E-GEOD-49977 | biostudies-arrayexpress

Activating c-KIT mutations confers oncogenic cooperativity and rescue RUNX1-ETO induced DNA-damage in human cells

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Activating c-KIT mutations confer oncogenic cooperativity and rescue RUNX1-ETO-induced DNA damage in human cells

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