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Hotspots of single-strand DNA "breakome" are enriched at transcriptional start sites of genes

ABSTRACT: Hotspots of single-strand DNA "breakome" are enriched at transcriptional start sites of genes

PROVIDER: PRJNA788284 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17208901_1.fastq.gz	Fastqsanger.gz
	SRR17208901_2.fastq.gz	Fastqsanger.gz
	SRR17208912_1.fastq.gz	Fastqsanger.gz
	SRR17208912_2.fastq.gz	Fastqsanger.gz
	SRR17208913_1.fastq.gz	Fastqsanger.gz

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Hotspots of single-strand DNA "breakome" are enriched at transcriptional start sites of genes

Project description:Single strand breaks (SSBs) represent one of the most common types of DNA damage yet not much is known about the genome landscapes of this type of DNA lesions in mammalian cells. Here, we found that SSBs are more likely to occur in certain positions of the human genome — SSB hotspots — in different cells of the same cell type and in different cell types. We hypothesize that the hotspots are likely to represent biologically relevant breaks. And, we found that the hotspots had a prominent tendency to be enriched in the immediate vicinity of transcriptional start sites (TSSs). We show that these hotspots are not likely to represent technical artifacts, or be caused by common mechanisms previously found to cause DNA cleavage at promoters, such as apoptotic DNA fragmentation or topoisomerase type II (TOP2) activity. Therefore, such TSS-associated hotspots could potentially be generated using a novel mechanism, that could involve preferential cleavage at cytosines, and their existence is consistent with recent studies suggesting a complex relationship between DNA damage and regulation of gene expression.

2022-08-18 | GSE190735 | GEO

Hotspots of single-strand DNA "breakome" are enriched at transcriptional start sites of genes.

Project description:Single-strand breaks (SSBs) represent one of the most common types of DNA damage, yet not much is known about the genome landscapes of this type of DNA lesions in mammalian cells. Here, we found that SSBs are more likely to occur in certain positions of the human genome-SSB hotspots-in different cells of the same cell type and in different cell types. We hypothesize that the hotspots are likely to represent biologically relevant breaks. Furthermore, we found that the hotspots had a prominent tendency to be enriched in the immediate vicinity of transcriptional start sites (TSSs). We show that these hotspots are not likely to represent technical artifacts or be caused by common mechanisms previously found to cause DNA cleavage at promoters, such as apoptotic DNA fragmentation or topoisomerase type II (TOP2) activity. Therefore, such TSS-associated hotspots could potentially be generated using a novel mechanism that could involve preferential cleavage at cytosines, and their existence is consistent with recent studies suggesting a complex relationship between DNA damage and regulation of gene expression.

| S-EPMC9420937 | biostudies-literature

CAGE mapping Drosophila Hemocytes start sites

Project description:CAGE mapping Drosophila Hemocytes start sites

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Common occurrence of hotspots of single strand DNA breaks at transcriptional start sites

Project description: Not available

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Neuronal Enhancers are Hotspots for DNA Single-Strand Break Repair

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

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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.

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

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

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

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Protein Determinants of Meiotic DNA Break Hotspots (dataset 2)

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 | GSE43121 | GEO

Protein Determinants of Meiotic DNA Break Hotspots (dataset 1)

2012-12-26 | GSE43118 | GEO