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Sexual dimorphism in the meiotic requirement for PRDM9: a mammalian evolutionary safeguard

ABSTRACT: Sexual dimorphism in the meiotic requirement for PRDM9: a mammalian evolutionary safeguard

PROVIDER: PRJNA602882 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12091146_1.fastq.gz	Fastqsanger.gz
	SRR12091146_2.fastq.gz	Fastqsanger.gz
	SRR12091147_1.fastq.gz	Fastqsanger.gz
	SRR12091147_2.fastq.gz	Fastqsanger.gz
	SRR12091148_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Sexual dimorphism in the meiotic requirement for PRDM9: a mammalian evolutionary safeguard

Project description:The locations of mammalian recombination hotspots are determined by PRDM9, a zinc finger histone methyltransferase that locally trimethylates histone H3 at residues K4 and K36. Here we report Prdm9-EP, a glu365pro mutation that severely reduces catalytic activity in vivo. This mutation causes sterility with complete meiotic arrest in homozygous males, while homozygous females are able to produce live offspring in natural matings. These H3K4me3 ChIP-seq data from Prdm9-EP homozygous spermatocytes show the extent to which H3K4 methyltransferase activity is compromised by this mutation, while the DMC1 ChIP-seq data show its effect on meiotic double-strand breaks in spermatocytes. For comparison, we mapped previously reported H3K4me3 ChIP-seq data from wild-type C57BL/6J spermatocytes (GSE52628) to mm10, merging the two biological replicates (SRX381465 and SRX381466) before mapping, and proceeding with processing. We did the same with published DMC1 ChIP-seq data, merging three previously reported DMC1 ChIP-seq biological replicates, isolated from wild-type C57BL/6N males (GSE112110; SRX3825301, SRX3825302, and SRX3825303). Processed data files are presented here.

2020-10-23 | GSE144144 | GEO

Sexual dimorphism in the meiotic requirement for PRDM9: A mammalian evolutionary safeguard.

Project description:In many mammals, genomic sites for recombination are determined by the histone methyltransferase PRMD9. Some mouse strains lacking PRDM9 are infertile, but instances of fertility or semifertility in the absence of PRDM9 have been reported in mice, canines, and a human female. Such findings raise the question of how the loss of PRDM9 is circumvented to maintain fertility. We show that genetic background and sex-specific modifiers can obviate the requirement for PRDM9 in mice. Specifically, the meiotic DNA damage checkpoint protein CHK2 acts as a modifier allowing female-specific fertility in the absence of PRDM9. We also report that, in the absence of PRDM9, a PRDM9-independent recombination system is compatible with female meiosis and fertility, suggesting sex-specific regulation of meiotic recombination, a finding with implications for speciation.

| S-EPMC7608834 | biostudies-literature

PRDM9 methyltransferase is essential for meiotic DSB formation

Project description:The programmed formation of hundreds DNA double strand breaks (DSBs) is essential for proper meiosis and fertility. In mice and humans, the location of these breaks is determined by the meiosis-specific protein PRDM9, through the DNA binding specificity of its zinc finger domain. PRDM9 also has methyltransferase activity. Here, we show that this activity is required for H3K4me3 and H3K36me3 deposition and for DSB formation at PRDM9 binding sites. By analyzing mice that express two PRDM9 variants with distinct DNA binding specificities, we reveal severalthe basic principles of PRDM9-dependent DSB site determination, in which an excess of sites are designated through PRDM9 binding and subsequent histone methylation, from which a subset are selected for DSB formation.

2018-02-09 | GSE108953 | GEO

Sexual dimorphism in mice

Project description:Sexual dimorphism in mice

| PRJEB2572 | ENA

Identification of PRDM9 partners

Project description:PRDM9 specifies the sites of meiotic DNA double strand break that initiate meiotic recombination in mice and humans. PRDM9 is known to bind to specific DNA sequences with its DNA binding domain, to induce H3K4me3 and H3K36me3 to adjacent nucleosomes through its methyltransferase activity, and to recruit or activate the meiotic DSB machinery. To understand how PRDM9 executes these various steps, we set up to identify its partners. This was performed by a proteomic approach where protein extracts from mouse testis were immunoprecipitated with anti-PRDM9 antibody for mass spectrometry analysis.

2020-12-03 | PXD017337 | Pride

The meiotic recombination activator PRDM9 trimethylates both H3K4 and H3K36 at recombination hotspots in vivo

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

Dual Histone Methyl Reader ZCWPW1 Facilitates Repair of PRDM9-Induced Meiotic Double Strand Breaks

Project description:Meiotic crossovers result from homology-directed repair of double strand breaks (DSBs). Unlike yeast and plants, where DSBs are generated near gene promoters, in many vertebrates, DSBs are enriched at hotspots determined by the DNA binding activity of the rapidly evolving zinc finger array of PRDM9 (PR domain zinc finger protein 9), which subsequently catalyzes trimethylation of lysine 4 and lysine 36 of Histone H3 in nearby nucleosomes. Here, we identify the dual histone methylation reader ZCWPW1, which is tightly co-expressed during spermatogenesis with Prdm9 and co-evolved with Prdm9 in vertebrates, as an essential meiotic recombination factor required for efficient synapsis and repair of PRDM9-dependent DSBs. In sum, our results indicate that the evolution of dual histone methylation reader/writer system involving Prdm9 and Zcwpw1 facilitated a shift in genetic recombination away from a static pattern near genes towards a flexible pattern controlled by the rapidly evolving DNA binding activity of PRDM9

2020-05-12 | GSE139289 | GEO

Sexual dimorphism in osteogenic differentiation

Project description:Sexual dimorphism in osteogenic differentiation

| PRJNA768873 | ENA

The meiotic recombination activator PRDM9 trimethylates both H3K4 and H3K36 at recombination hotspots in vivo

2016-06-30 | GSE76416 | GEO

Sexual dimorphism in gene expression in two species of songbirds

Project description:We have done an expression experiment studying sexual dimorphism in gene expression in two species of songbirds, the zebra finch (Teaniopigia guttata) and the common whitethroat (Sylvia communis).

2010-11-30 | E-MEXP-2914 | biostudies-arrayexpress

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