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Genome-wide binding site of Rec10 and Rec15 during meiosis

ABSTRACT: Higher-order chromosome structure is assumed to control various DNA-templated reactions in eukaryotes. Meiotic chromosomes implement developed structures called “axes” and “loops”; both are suggested to tether each other, activating Spo11 to catalyze meiotic DNA double-strand breaks (DSBs) at recombination hotspots. We found that the Schizosaccharomyces pombe Spo11 homolog Rec12 and its partners form two distinct subcomplexes, DSBC (Rec6-Rec12-Rec14) and SFT (Rec7-Rec15-Rec24). Additionally, Mde2, whose expression is strictly regulated by the replication checkpoint, interacts with a component of each subcomplex. The SFT subcomplex binds to both axes via direct interaction of Rec15 with Rec10 in axes and DSB sites, hence axial Rec10 can partially tether DSB sites located in loops. Importantly, this multiprotein-based tethered axis-loop complex is destabilized in the absence of Mde2. We therefore propose a novel mechanism by which Mde2 functions as a recombination initiation mediator to tether axes and loops, in liaison with the meiotic replication checkpoint.

ORGANISM(S): Schizosaccharomyces pombe

PROVIDER: GSE31846 | GEO | 2012/07/28

SECONDARY ACCESSION(S): PRJNA145103

REPOSITORIES: GEO

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Genome-wide binding site of Rec10 and Rec15 during meiosis

Project description:Higher-order chromosome structure is assumed to control various DNA-templated reactions in eukaryotes. Meiotic chromosomes implement developed structures called M-bM-^@M-^\axesM-bM-^@M-^] and M-bM-^@M-^\loopsM-bM-^@M-^]; both are suggested to tether each other, activating Spo11 to catalyze meiotic DNA double-strand breaks (DSBs) at recombination hotspots. We found that the Schizosaccharomyces pombe Spo11 homolog Rec12 and its partners form two distinct subcomplexes, DSBC (Rec6-Rec12-Rec14) and SFT (Rec7-Rec15-Rec24). Additionally, Mde2, whose expression is strictly regulated by the replication checkpoint, interacts with a component of each subcomplex. The SFT subcomplex binds to both axes via direct interaction of Rec15 with Rec10 in axes and DSB sites, hence axial Rec10 can partially tether DSB sites located in loops. Importantly, this multiprotein-based tethered axis-loop complex is destabilized in the absence of Mde2. We therefore propose a novel mechanism by which Mde2 functions as a recombination initiation mediator to tether axes and loops, in liaison with the meiotic replication checkpoint. ChIP-chip analyses of Rec10 (in wild type), Mde2 (in wild type and rec15M-bM-^HM-^F), and Rec15 (in wild type, rec10M-bM-^HM-^F, rec24M-bM-^HM-^F and mde2M-bM-^HM-^F) at meiosis 4 hours.

2012-07-27 | E-GEOD-31846 | biostudies-arrayexpress

Spp1, a member of Set1 complex, promotes meiotic DSB formation by tethering histone H3K4 methylation sites to chromosome axes

Project description:Meiotic DSB, catalyzed by the Spo11 transesterase protein and accessory DSB proteins, form in the nucleosome depleted regions (NDR) at promoters, preferentially those located on the chromosome loops that shape meiotic chromosomes, whereas the DSB proteins are located on chromosome axes at the basis of these loops. Mechanisms bridging these two chromosomal regions for DSB formation have remained elusive. Here we show that Spp1, a conserved member of the histone H3K4 methyltransferase Set1 complex, is required for normal levels of DSB formation and is associated with chromosome axes in the DSB-rich domains during meiosis. Moreover, Spp1 physically interacts with the Mer2 axis-associated DSB protein, and uses its PHD finger as a magnet to read H3K4 trimethylation close to promoters, tether these regions to chromosome axes and activate cleavage in the nearby promoter by the DSB proteins. We further show that in the absence of Spp1 or the Set1 complex, DSB are introduced at a few new sites, located in promoters of transcriptionally induced genes, suggesting another selection mechanism of preferred DSB sequences. This paper provides the molecular mechanism linking H3K4me3 to the DSB forming machinery, by the meiosis-specific specialization of Spp1 as an active member of the DSB complex and a reader of H3K4me3, and opens perspectives for the study of DSB formation at mammalian recombination hotspots that are also enriched in H3K4me3. ChIP-chip experiment in vegetative or meiotic diploid SK1 yeast cells - two biological replicates

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Spp1, a member of Set1 complex, promotes meiotic DSB formation by tethering histone H3K4 methylation sites to chromosome axes

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2023-05-01 | GSE221033 | GEO

Mapping of Rec12 oligonucleotides in Schizosaccharomyces pombe

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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

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Project description:Histone modifications are associated with meiotic recombination hotspots, discrete sites with augmented recombination frequency. For example, trimethylation of histone H3 lysine4 (H3K4me3) marks most hotspots in budding yeast and mouse. Modified histones are known to regulate meiotic recombination partly by promoting DNA double strand break (DSB) formation, but the role and precise landscape of histone modifications at hotspots remain unclear. Here, we studied hotspot-associated modifications in fission yeast and found general features: acetylation of H3 lysine9 (H3K9ac) is strikingly elevated, and H3K4me3 is not significantly enriched. Remarkably, elimination of H3K9ac reduced binding of the DSB-inducing enzyme Rec12 and DSB at hotspots. We also found that the H3K4 metyltransferase Set1 promotes DSB formation at some loci, but it restricts Rec12 binding to hotspots. These results suggest that H3K9ac rather than H3K4me3 is a hotspot-associated mark involved in meiotic DSB formation in fission yeast.

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