Functional Roles of Acetylated Histone Marks at Mouse Meiotic Recombination Hotspots
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ABSTRACT:
PROVIDER: PRJNA343465 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR4255680.fastq.gz | Fastqsanger.gz | |||
| SRR4255676.fastq.gz | Fastqsanger.gz | |||
| SRR4255677.fastq.gz | Fastqsanger.gz | |||
| SRR4255678.fastq.gz | Fastqsanger.gz | |||
| SRR4255679.fastq.gz | Fastqsanger.gz |
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Project description:Meiotic recombination is initiated by the Spo11 endonuclease, which directs DNA DSBs. We report here that the recombinogenic cores of active hotspots in mice harbor several histone H3 and H4 acetylation and methylation marks that are typical of open, active chromatin. Further, deposition of these histone marks is dynamic and manifest at spermatogonia and/or pre-leptotene meiotic cells, which would facilitate the formation of DSBs at leptotene. Importantly, there was concordance in the overlap of the histone mark ChIP profiles with nucleosome occupancy maps, which were determined by real-time PCR and whole genome sequencing (WGS) analyses of micococcal-nuclease resistance regions across four mouse meiotic hotspots (HS22, HS59.4, HS59.5 and HS61.1). Our study reveals that there are instructive roles of histone acetylated marks at meiotic recombination hotspot cores and that they are necessary to promote hotspot activity and crossover resolution.
2016-11-04 | GSE87057 | GEO
Project description:Meiotic recombination is initiated by the Spo11 endonuclease, which directs DNA double strand breaks at discrete regions in the genome coined hotspots. Here we report the profiles and dynamics of histone modifications at the cores of mouse recombination hotspots in early meiotic prophase. To define the spectrum of possible regulators of histone methylation and acetylation at all stages of meiosis I, expression analyses of histone acetylases/deacetylases (HATs/HDACs) and and HMTs/HDMTs genes when comparing those expressed in spermatogonia, pre-leptotene and leptotene/zygotene versus pachytene meiotic stages.
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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.
2013-03-07 | GSE31648 | GEO
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. S.pombe cells in a pat1-114 background were induced to enter meiosis by the haploid meiosis system, and harvested one hour after the induction. ChIP were performed using anti-H3Cter, H3K9ac, -H3K14ac and -H3K4me3 antibodies. pat1-114 rad50S rec12+-FLAG cells in a wild type, H3K9A or set1+ deletion background were induced to enter meiosis by the haploid meiosis system, and harvested five hours after the induction. ChIP were performed using anti-FLAG antibodies.
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Project description:To determine meiotic recombination initiation sites in Arabidopsis thaliana genome we purified and sequenced oligonucleotides (35-45 nt) bound to SPO11-1, meiosis specific transesterase that induces meiotic DSB formation. This reveals that SPO11-1-oligonucleotide hotspots occur at nucleosome depleted regions of gene promoters, introns, terminators and specific families of DNA transposons (recomposons). To investigate the influence of chromatin structure and epigenetic factors on meiotic DSB formation we performed sequencing of SPO11-1-oligonucleotides in arp6, met1 and suvh4 suvh5 suvh6.
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Project description:In many eukaryotes, meiotic recombination occurs preferentially at discrete sites, called recombination hotspots. In various lineages, recombination hotspots are located in regions with promoter-like features and are evolutionarily stable. Conversely, in some mammals, hotspots are driven by PRDM9 that targets recombination away from promoters. Paradoxically, PRDM9 induces the self-destruction of its targets and this triggers an ultra-fast evolution of mammalian hotspots. PRDM9 is ancestral to all animals, suggesting a critical importance for the meiotic program, but has been lost in many lineages with surprisingly little effect on meiosis success. However, it is unclear whether the function of PRDM9 described in mammals is shared by other species. To investigate this, we analyzed the recombination landscape of several salmonids, the genome of which harbors one full-length PRDM9 and several truncated paralogs. We identified recombination initiation sites in Oncorhynchus mykiss by mapping meiotic DNA double-strand breaks (DSBs). We found that DNA DSBs clustered at hotspots positioned away from promoters, enriched for the H3K4me3 and H3K36me3 marks and the location of which depended on the genotype of full-length Prdm9. We observed a high level of polymorphism in the zinc finger domain of full-length Prdm9, indicating diversification driven by positive selection. Moreover, population-scaled recombination maps in O. mykiss, Oncorhynchus kisutch and Salmo salar revealed a rapid turnover of recombination hotspots caused by PRDM9 target motif erosion. Our results imply that PRDM9 function is conserved across vertebrates and that the peculiar evolutionary runaway caused by PRDM9 has been active for several hundred million years.
2024-09-23 | GSE277449 | GEO
Project description:Meiotic recombination differs between males and females, however, when and how these differences are established is unknown. We identify extensive sex differences at recombination initiation by mapping hotspots of meiotic DNA double strand breaks in male and female mice. Contrary to past findings in humans, few hotspots are used uniquely in either sex. Instead, grossly different recombination landscapes result from up to 15-fold differences in hotspot use between males and females. Indeed, most recombination occurs at sex-biased hotspots. Sex biased hotspots appear to be partly determined by chromosome structure, and DNA methylation, absent in females at the onset of meiosis, plays a substantial role. Sex differences are also evident later in meiosis as the repair frequency of distal meiotic breaks as crossovers diverges in males and females. Suppression of distal crossovers may help to minimize age-related aneuploidy that arises due to cohesion loss during dictyate arrest in females.
2018-09-20 | GSE99921 | GEO
Project description:Mammalian genetic recombination is concentrated at hotspots, specialized 1-2 Kb sites separated by long stretches of DNA lacking recombination. Mammalian hotspot locations depend on PRDM9, a zinc finger protein that binds at hotspots and uses its SET domain to locally trimethylate histone H3K4. Here we find that PRDM9 also locally trimethylates H3K36 at hotspots. Using ChIP-seq and immunoprecipitation data for H3K36me3 in murine spermatocytes, we show that H3K4me3 and H3K36me3 coincide only at hotspots in germ cells, and that this H3K4me3/H3K36me3-double-positive signature is almost entirely dependent on PRDM9.
2016-06-30 | GSE76416 | GEO
Project description:In Schizosaccharomyces pombe, DNA replication origins (ORIs) and meiotic recombination hotspots lack consensus sequences and show a bias towards mapping at large intergenic regions (IGRs). To explore whether this preference depended on underlying chromatin features, we have generated genome-wide nucleosome profiles during mitosis and meiosis. We have found that meiotic double-strand break sites (DSB) colocalize strictly with nucleosome-depleted regions (NDRs) and that large IGRs include clusters of NDRs that overlap with almost half of all DSBs. By contrast, ORIs do not colocalize with NDRs and they are regulated independently of DSBs. Physical relocation of NDRs at ectopic loci or modification of their genomic distribution during meiosis was paralleled by the generation of new DSB sites. Over 80% of all meiotic DSBs colocalize with NDRs that are also present during mitosis, indicating that the recombination pattern is largely dependent on constitutive properties of the genome and, to a lesser extent, on the transcriptional profile during meiosis. The organization of ORIs and of DSBs regions in S. pombe reveals similarities and differences relative to Saccharomyces cerevisiae.
2011-12-31 | GSE28879 | GEO
Project description:Mammalian genetic recombination is concentrated at hotspots, specialized 1-2 Kb sites separated by long stretches of DNA lacking recombination. Mammalian hotspot locations depend on PRDM9, a zinc finger protein that binds at hotspots and uses its SET domain to locally trimethylate histone H3K4. Here we find that PRDM9 also locally trimethylates H3K36 at hotspots. Using ChIP-seq and immunoprecipitation data for H3K36me3 in murine spermatocytes, we show that H3K4me3 and H3K36me3 coincide only at hotspots in germ cells, and that this H3K4me3/H3K36me3-double-positive signature is almost entirely dependent on PRDM9. We performed ChIP-seq with an antibody against H3K36me3, using chromatin extracted from murine spermatocytes, and compared it to previously generated ChIP-seq data for H3K4me3 in the same cell type. ---------------------------------- This dataset represents the H3K36 component only
2016-06-30 | E-GEOD-76416 | biostudies-arrayexpress