Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genomic features shaping the landscape of meiotic double-strand break hotspots in maize

ABSTRACT: Genomic features shaping the landscape of meiotic double-strand break hotspots in maize

PROVIDER: PRJNA328981 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR1185590.fastq.gz	Fastqsanger.gz
	SRR1185582.fastq.gz	Fastqsanger.gz
	SRR1185583.fastq.gz	Fastqsanger.gz
	SRR1185584.fastq.gz	Fastqsanger.gz
	SRR1185585.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 11

Similar Datasets

Genomic features shaping the landscape of meiotic double-strand break hotspots in maize [ChIP-Seq]

Project description:To generate the double-strand break (DSB) hotspot map in maize, we used a chromatin immunoprecipitation (ChIP) approach, in which chromatin from flowers containing zygotene meiocytes was enriched in fragments associated with RAD51.

2016-07-08 | GSE55701 | GEO

Protein Determinants of Meiotic DNA Break Hotspots (dataset 1)

Project description:Meiotic recombination, crucial for proper chromosome segregation and genome evolution, is initiated by programmed DNA double-strand breaks (DSBs) in budding and fission yeasts and likely all sexually reproducing species. In fission yeast, DSBs occur up to several hundred times more frequently at special sites, called hotspots, than in other regions of the genome. What distinguishes hotspots from cold regions is a major unsolved problem, although transcription factors determine some hotspots. We report here the discovery that three coiled-coil proteins -- Rec25, Rec27, and Mug20 -- bind essentially all hotspots with unprecedented, high specificity even without DSB formation. These small proteins are components of linear elements, are related to synaptonemal complex proteins, and are essential for nearly all DSBs at most hotspots. Our results indicate that these hotspot determinants activate or stabilize the DSB-forming protein Rec12 (Spo11 homolog) rather than promote its binding to hotspots. We propose here a new paradigm for hotspot determination and crossover control by linear element proteins.

2012-12-26 | GSE43118 | GEO

Protein Determinants of Meiotic DNA Break Hotspots (dataset 2)

2012-12-26 | GSE43121 | GEO

Neuronal Enhancers are Hotspots for DNA Single-Strand Break Repair

Project description:Neuronal Enhancers are Hotspots for DNA Single-Strand Break Repair

| PRJNA704019 | ENA

Neuronal Enhancers are Hotspots for DNA Single-Strand Break Repair [SEAL]

Project description:Neuronal Enhancers are Hotspots for DNA Single-Strand Break Repair [SEAL]

| PRJNA704028 | ENA

Neuronal Enhancers are Hotspots for DNA Single-Strand Break Repair [HiC]

Project description:Neuronal Enhancers are Hotspots for DNA Single-Strand Break Repair [HiC]

| PRJNA704022 | ENA

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

In vitro reconstitution of meiotic DNA double-strand break formation

Project description:In vitro reconstitution of meiotic DNA double-strand break formation

| PRJNA1184718 | ENA

Meiotic double-strand break mapping in spo11 mutants by S1Seq

Project description:Meiotic double-strand break mapping in spo11 mutants by S1Seq

| PRJNA631754 | ENA

Meiotic prophase length modulates Tel1-dependent DNA double-strand break interference

Project description:During meiosis, genetic recombination is initiated by the formation of many DNA double-strand breaks (DSBs) catalysed by the evolutionarily conserved topoisomerase-like enzyme, Spo11, in preferred genomic sites known as hotspots. DSB formation activates the Tel1/ATM DNA damage responsive (DDR) kinase, locally inhibiting Spo11 activity in adjacent hotspots via a process known as DSB interference. Intriguingly, in S. cerevisiae, over short genomic distances (<15 kb), Spo11 activity displays characteristics of concerted activity or clustering, wherein the frequency of DSB formation in adjacent hotspots is greater than expected by chance. We have proposed that clustering is caused by a limited number of sub-chromosomal domains becoming primed for DSB formation. Here, we provide evidence that DSB clustering is abolished when meiotic prophase timing is extended via deletion of the NDT80 transcription factor. We propose that extension of meiotic prophase enables most cells, and therefore most chromosomal domains within them, to reach an equilibrium state of similar Spo11-DSB potential, reducing the impact that priming has on estimates of coincident DSB formation. Consistent with this view, when Tel1 is absent but Ndt80 is present and thus cells are able to rapidly exit meiotic prophase, genome-wide maps of Spo11-DSB formation are skewed towards pericentromeric regions and regions that load pro-DSB factors early—revealing regions of preferential priming—but this effect is abolished when NDT80 is deleted. Our work highlights how the stochastic nature of Spo11-DSB formation in individual cells within the limited temporal window of meiotic prophase can cause localised DSB clustering—a phenomenon that is exacerbated in tel1∆ cells due to the dual roles that Tel1 has in DSB interference and meiotic prophase checkpoint control.

2023-10-18 | GSE245327 | GEO

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