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H3K4me3 ChIP-seq from B6CASTF1-PRDM9 Humanized/CAST testes

ABSTRACT: H3K4me3 ChIP-seq from B6CASTF1-PRDM9 Humanized/CAST testes

PROVIDER: PRJNA490145 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7814097_1.fastq.gz	Fastqsanger.gz
	SRR7814097_2.fastq.gz	Fastqsanger.gz
	SRR7814098_1.fastq.gz	Fastqsanger.gz
	SRR7814098_2.fastq.gz	Fastqsanger.gz
	SRR7814099_1.fastq.gz	Fastqsanger.gz

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H3K4me3 ChIP-seq from B6CASTF1-PRDM9 Humanized/CAST testes

Project description:We report testis H3K4me3 enrichment in an F1 male from a C57BL/6J (B6) x CAST/Eij (CAST) cross (B6 mother, CAST father). This mouse is heterozygous at PRDM9 for a humanized allele (Davies et al. Nature 2016) and the CAST allele. After filtering of promoter H3K4me3 regions, these data serve as a measure of PRDM9 binding enrichment on each homologue. We found that both crossovers and non-crossovers (observed by sequencing F2/F4/F5 genomic DNA) are depleted at "asymmetric" Double-Strand Break hotspots where PRDM9 primarily binds only one of the two homologues. This proves that PRDM9 plays an important role in promoting inter-homologue interactions and can explain why increasing PRDM9 binding asymmetry predicts hybrid infertility. See Li, Bitoun, Altemose et al. 2018 (pending) for a complete summary.

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B6xCAST F1 PRDM9-Humanized/CAST testes

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Crossovers from B6xCAST F1 PRDM9-Humanized/CAST testes

Project description:We report 2,649 crossover breakpoints identified by single-cell DNA sequencing of 217 sperm in a B6xCAST F1 mouse, which is heterozygous at Prdm9, with one wild-type CAST allele and one allele found in human populations (bred from a genetically engineered mother, Davies et al Nature 2012). Separately, we have reported testis DMC1 enrichment in the same mouse (GSE124991). We also infer H3K4me3 intensities at DMC1 hotspots, based on the raw H3K4me3 ChIP-seq data published under GSE119727 (Li et al). We identify several factors, including PRDM9 binding on the repair-template homologue, telomere proximity and local GC-content, that affect the probability that a DSB is repaired as a crossover. We further show that these factors also influence the time it takes for the site of a DSB to find and engage its homologue, with rapidly-engaging sites being more likely to be repaired as crossovers.

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Project description:We report testis DMC1 enrichment at DSB (Double-Strand Break) hotspots in a B6xCAST F1 mouse, which is heterozygous at Prdm9, with one wild-type CAST allele and one allele found in human populations (bred from genetically engineered mother, Davies et al Nature 2012). We also report H3K4me3 intensities at these hotspots, based on the raw data published under GSE119727 (Li et al). Separately, we have reported 2,649 crossover locations identified by single-cell DNA sequencing of 217 sperm from the same hybrid mouse. We identify several factors, including PRDM9 binding on the repair-template homologue, telomere proximity and local GC-content, that affect the probability that a DSB is repaired as a crossover. We further show that these factors also influence the time it takes for the site of a DSB to find and engage its homologue, with rapidly-engaging sites being more likely to be repaired as crossovers.

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Project description:We report testis H3K4me3 and DMC1 enrichment at DSB hotspots in various mice to examine differences between infertile hybrid mice and mice that have been humanized at PRDM9, which have rescued fertility. We find that infertile mice have an excess of "asymmetric" DSB hotspots, where both H3K4me3 and DMC1 reads tend to originate from only one homologue. At these hotspots, we see an excess of DMC1 relative to H3K4me3, consistent with delayed DSB repair at these sites. See Davies et al. Nature 2016 for a complete summary.

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Project description:This SuperSeries is composed of the SubSeries listed below.

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