Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA301682 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2932470.fastq.gz | Fastqsanger.gz | |||
| SRR2932470_1.fastq.gz | Fastqsanger.gz | |||
| SRR2932470_2.fastq.gz | Fastqsanger.gz | |||
| SRR2932471_1.fastq.gz | Fastqsanger.gz | |||
| SRR2932471_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 13 |
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Project description:DNA double-strand breaks (DSBs) and their repair can cause extensive epigenetic changes. As a result, DSBs have been proposed to promote transcriptional and, ultimately, physiological dysfunction via both cell-intrinsic and cell-non-autonomous pathways. Studying the consequences of DSBs in higher organisms has, however, been hindered by a scarcity of tools for controlled DSB induction. Using a mouse model for both tissue-specific and temporally controlled DSB formation, we investigated the transcriptional response to break repair. Transcriptional profiling of lymphocytes in spleen and thymus by RNA-Seq, with and without I-PpoI knock-in.
2016-01-04 | E-GEOD-74855 | biostudies-arrayexpress
Project description:DNA double strand breaks (DSBs) in B lymphocytes are thought to arise stochastically during replication (S phase) or as a result of targeted DNA damage by activation induced cytidine deaminase (AID) in G1. Here we identify a novel class of recurrent, early replicating and AID independent DNA lesions, termed early replication fragile sites (ERFS), by genome-wide localization of DNA repair proteins DNA double strand breaks (DSBs) in B lymphocytes are thought to arise stochastically during replication (S phase) or as a result of targeted DNA damage by activation induced cytidine deaminase (AID) in G1. Here we identify a novel class of recurrent, early replicating and AID independent DNA lesions, termed early replication fragile sites (ERFS), by genome-wide localization of DNA repair proteins DNA double strand breaks (DSBs) in B lymphocytes are thought to arise stochastically during replication (S phase) or as a result of targeted DNA damage by activation induced cytidine deaminase (AID) in G1. Here we identify a novel class of recurrent, early replicating and AID independent DNA lesions, termed early replication fragile sites (ERFS), by genome-wide localization of DNA repair proteins RPA, SMC5, gamma-H2AX, and BRCA1 in B cells subjected to replication stress. Protein-DNA association for four DNA damage response proteins (RPA, SMC5, g-H2AX, BRCA1), BrdU incorporation, and gene transcription in B lymphocytes with and without hydroxyurea treatment were examined.
2013-02-04 | E-GEOD-43504 | biostudies-arrayexpress
Project description:DNA double strand breaks (DSBs) in B lymphocytes are thought to arise stochastically during replication (S phase) or as a result of targeted DNA damage by activation induced cytidine deaminase (AID) in G1. Here we identify a novel class of recurrent, early replicating and AID independent DNA lesions, termed early replication fragile sites (ERFS), by genome-wide localization of DNA repair proteins DNA double strand breaks (DSBs) in B lymphocytes are thought to arise stochastically during replication (S phase) or as a result of targeted DNA damage by activation induced cytidine deaminase (AID) in G1. Here we identify a novel class of recurrent, early replicating and AID independent DNA lesions, termed early replication fragile sites (ERFS), by genome-wide localization of DNA repair proteins DNA double strand breaks (DSBs) in B lymphocytes are thought to arise stochastically during replication (S phase) or as a result of targeted DNA damage by activation induced cytidine deaminase (AID) in G1. Here we identify a novel class of recurrent, early replicating and AID independent DNA lesions, termed early replication fragile sites (ERFS), by genome-wide localization of DNA repair proteins RPA, SMC5, gamma-H2AX, and BRCA1 in B cells subjected to replication stress.
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Project description:Recent studies suggest that the repair of DNA double-strand breaks (DSBs) is supported by damage-induced small RNAs (diRNAs) that are generated by Drosha and Dicer from transcripts that originate from the regions flanking the break. However, transcription and diRNA production at naturally occurring DSBs in mammalian genomes remain controversial. We have used the homing endonuclease I-PpoI to produce DSBs in human and mouse cells, and we have analyzed the biogenesis of diRNAs at I-PpoI induced breaks in the 28S rDNA and the Ryr2 gene. We provide direct evidence that RNA polymerase II transcribes the sequences that flank the DSBs. Our results also reveal that the resulting transcripts are processed into two types of diRNAs with characteristic length and terminal nucleotide signatures. Furthermore, diRNA production is independent of Drosha and DGCR8, and only a subset of diRNAs depends on Dicer, as shown by small RNA analyses of knock-out cells that lack specific RNA processing enzymes. Our findings are compatible with previous observations of a general transcription inhibition at DSBs and provide novel insights into the mechanisms of RNA synthesis and processing at DSBs.
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Project description:In depth analysis of double strand break signaling was performed using mouse Pre-B cells and Human HCT116 cells. Our analysis included the induction of double strand breaks with ionizing radiation with the addition of ATM and DNA-PKcs inhibitors, alone and in combination.
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Project description:High concentration of NaCl increases DNA breaks both in cell culture and in vivo. The breaks remain elevated as long as NaCl concentration remains high and are rapidly repaired when the concentration is lowered. Repair of the breaks after NaCl is reduced is accompanied by formation of foci containing phosphorylated H2AX (γH2AX), which occurs around DNA double-strand breaks and contributes to their repair. By chromatin immunoprecipitation using anti-γH2AX antibody, followed by massive parallel sequencing (ChIP-Seq), we find that during repair of double–strand breaks induced by high NaCl, γH2AX is predominantly localized to regions of the genome devoid of genes (“gene deserts”), indicating that the high NaCl-induced double-strand breaks are located there. Localization to gene deserts helps explain why the DNA breaks are less harmful than are the random breaks induced by genotoxic agents such as UV radiation, ionizing radiation and oxidants. We propose that the universal presence of NaCl around animal cells has directly influenced the evolution of the structure of their genomes.
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