Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA111625 | ENA |
REPOSITORIES: ENA
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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.
2011-11-21 | GSE32882 | GEO
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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 (M-NM-3H2AX), which occurs around DNA double-strand breaks and contributes to their repair. By chromatin immunoprecipitation using anti-M-NM-3H2AX antibody, followed by massive parallel sequencing (ChIP-Seq), we find that during repair of doubleM-bM-^@M-^Sstrand breaks induced by high NaCl, M-NM-3H2AX is predominantly localized to regions of the genome devoid of genes (M-bM-^@M-^\gene desertsM-bM-^@M-^]), 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. ChIP-Seq experiment to find locations of M-NM-3H2AX in mouse genome
2011-11-21 | E-GEOD-32882 | biostudies-arrayexpress
Project description:Nucleic Acid Sequencing for the study of division induced double strand breaks in the terminus region of Escherichia coli cells lacking RecBCD DNA repair enzymes.
2017-09-18 | E-MTAB-6030 | biostudies-arrayexpress
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.
2024-10-17 | PXD042258 | Pride
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.
2013-02-04 | GSE43504 | GEO
Project description:Protein post-translational modification (PTM) plays a central role in the DNA damage response. In particular protein phosphorylation and ubiquitination have been shown to play a major role in the signalling cascade that coordinates break repair with cell cycle progression. Here we performed large-scale quantitative proteomics to identify changes in protein ubiquitination that are induced by DNA double-strand breaks. In total we quantified >9400 ubiquitin sites, and found that the relative abundance of ~10% of these sites was altered in response to DNA double-strand breaks. Interestingly, we found a large proportion of the ribosomal proteins to be ubiquitinated after damage. These included ribosomal proteins from the 40S as well as the 60S subunit. We subsequently show that DNA damage damage leads to a transient inhibition in ribosome function in protein synthesis. Taken together, these data uncover ribosome ubiquitination as a consequence of activation of the DDR .
2018-02-23 | PXD004445 | Pride