Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mus musculus

ABSTRACT: The landscape of mouse meiotic double-strand break formation, processing and repair

PROVIDER: PRJNA330844 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR3939690_1.fastq.gz	Fastqsanger.gz
	SRR3939690_2.fastq.gz	Fastqsanger.gz
	SRR3939691_1.fastq.gz	Fastqsanger.gz
	SRR3939691_2.fastq.gz	Fastqsanger.gz
	SRR3939692_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 10

Similar Datasets

EWSR1 regulates PRDM9-dependent histone 3 methylation and links recombinant hotspots to the chromosomal axis

Project description:Meiotic recombination in mammals requires recombination hotspot activation through the action of the histone 3 lysine-4 and lysine-36 methyltransferase PRDM9 to ensure successful double-strand break initiation and repair. Here using a Ewsr1 male germ cell conditional knockout mouse, we show that EWSR1 increases the efficiency of PRDM9-dependent H3K4/K36 trimethylation at the adjacent nucleosomes in vivo, and directs the hotspot choices for double-strand breaks formation and their subsequent repair into sufficient number of crossovers properly positioned along the centromere-telomere axis.

2020-12-17 | GSE108259 | GEO

FIGNL1 AAA+ ATPase remodels RAD51 and DMC1 filaments in meiotic DNA replication and recombination

Project description:The formation of RAD51/DMC1 filaments on single-stranded (ss)DNAs, which is essential for homology search and strand exchange in DNA double-strand break (DSB) repair and for the protection of stalled DNA replication forks, is tightly regulated in time and space. FIGNL1 AAA+++ ATPase plays positive and negative roles in the RAD51-mediated recombination in human cells. However, the role of FIGNL1 in gametogenesis remains unsolved. Here, we characterized a germ-line-specific conditional knockout (cKO) mouse of FIGNL1. The Fignl1 cKO male mice showed defective chromosome synapsis and impaired meiotic DSB repair with the accumulation of RAD51/DMC1 on chromosomes in mid-meiotic prophase I, supporting a role of FIGNL1 in a post-assembly stage of RAD51/DMC1 filaments. Fignl1 cKO spermatocytes accumulate RAD51 and DMC1 ensembles on chromosomes not only in early meiotic prophase I but also in meiotic S-phase. These RAD51/DMC1 assemblies are independent of meiotic DSB formation. Finally, we showed that purified FIGNL1 dismantles RAD51 filament on double-stranded (ds)DNA as well as ssDNA. These results suggest a critical role of FIGNL1 to limit the uncontrolled assembly of RAD51 and DMC1 on native dsDNAs during the meiotic S-phase and meiotic prophase I.

2023-03-31 | GSE227944 | GEO

ANKRD31 protein interactions

Project description:Sex chromosomes in males of most mammalian species share only a small homologous segment, the pseudoautosomal region (PAR), wherein double-strand break (DSB) formation must occur for correct meiotic segregation. We find that multiple DSB-promoting factors hyperaccumulate in the PAR, including the ankyrin-repeat domain-containing protein ANKRD31. We used immunoprecipitation and mass spectrometry from extracts of juvenile mouse testes to identify potential ANKRD31-interacting proteins.

2020-06-19 | PXD017191 | Pride

Distribution of Holliday Junctions and Repair Forks during Escherichia coli DNA Double-Strand Break Repair

Project description:Here, we correlated and compared two different steps of the Double-Strand Break Repair pathway: RecA loading and Holliday junction formation

2021-07-29 | GSE179963 | GEO

Project description:Repair-seq screens of double-strand break repair

| PRJNA746980 | ENA

DEtail-seq profiled meiotic DSBs in Mus musculus

Project description:SPO11-promoted DNA double-strand breaks (DSBs) formation is a crucial step for meiotic recombination, and it is indispensable to detect the broken DNA ends accurately for dissecting the molecular mechanisms behind. Here, we report a novel technique, named DEtail-seq (DNA End tailing followed by sequencing), that can directly and quantitatively capture the meiotic DSB 3’ overhang hotspots at single-nucleotide resolution.

2023-01-08 | GSE154289 | GEO

CXXC1 is not essential for normal DNA double-strand break formation and meiotic recombination in mouse

Project description:In most mammals, including mice and humans, meiotic recombination is determined by the meiosis specific histone methytransferase PRDM9, which binds to specific DNA sequences and trimethylates histone 3 at lysine-4 and lysine-36 at the adjacent nucleosomes. These actions ensure successful DNA double strand break formation and repair that occur on the proteinaceous structure forming the chromosome axis. The process of hotspot association with the axis after their activation by PRDM9 is poorly understood. Previously, we and others have identified CXXC1, an ortholog of S. cerevisiae Spp1 in mammals, as a PRDM9 interactor. In yeast, Spp1 is a histone methyl reader that links H3K4me3 sites with the recombination machinery, promoting DSB formation. Here, we investigated whether CXXC1 has a similar function in mouse meiosis. We created two Cxxc1 conditional knockout mouse to deplete CXXC1 generally in germ cells, and before the onset of meiosis. Surprisingly, male knockout mice were fertile, and the loss of CXXC1 in spermatocytes had no effect on hotspot trimethylation, double-strand break formation or repair. Our results demonstrate that CXXC1 is not an essential link between PRDM9-activated recombination hotspot sites and DSB machinery and that the hotspot recognition pathway in mouse is independent of CXXC1.

2018-08-29 | GSE116336 | GEO

Whole-genome nucleosome mapping in meiotic diploid S. cerevisiae

Project description:We determined nucleosome positions throughout the genome in diploid S. cerevisiae undergoing early stages of synchronous meiosis. This study sought to assess if systematic reorganization of nucleosomes occurs during meiotic prophase at or near sites of DNA double strand break formation.

2011-03-07 | GSE26452 | GEO

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

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

Recombination initiation maps of individual human genomes

Project description:DNA double-strand breaks (DSBs) are introduced in meiosis to initiate recombination and to generate crossovers, the reciprocal exchanges of genetic material between parental chromosomes. Here we present the first high-resolution map of meiotic DSBs in individual human genomes. Comparing DSB maps between individuals shows that along with DNA binding by PRDM9, additional factors dictate the efficiency of DSB formation. Furthermore, we find that in human males, the frequency of DSB formation is the primary determinant of crossover rate. Patterns of sequence polymorphisms around meiotic DSB hotspots provide evidence for both GC-biased gene conversion and for a mutagenic role of DSB repair and/or recombination. Finally, we provide compelling evidence that the aberrant repair of meiotic DSBs is a driver of human genomic disorders. Detection of meiotic double strand breaks in testis of several human male individuals.

2014-11-17 | E-GEOD-59836 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data