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Expression data for program activation by IR-induced DNA breaks in G1 phase Murine PreB cells

ABSTRACT: The objective of this set of samples is to identify genes that are differentially expressed following the introduction of DNA double strand breaks (DSBs) by ionizing radiation in wild-type murine pre-B cells. The data generated in this project will be compared to the data generated in GSE9024, in which genes that are differentially expressed following the introduction of DNA double strand breaks (DSBs) by the Rag proteins in murine pre-B cells were examined. In order to understand the differences between the physiologic and genotoxic responses to DSB DNA damage, we need to compare cells that are all in the same compartment of the cell cycle. We are therefore examining the response to IR-induced damage in cells that are arrested in G1, which would correspond to our previous study of G1 arrested cells with Rag-induced breaks. This will illuminate the difference directly, allowing us to better understand the signaling responses to the different types of DNA damage.

ORGANISM(S): Mus musculus

PROVIDER: GSE36530 | GEO | 2013/03/13

SECONDARY ACCESSION(S): PRJNA153399

REPOSITORIES: GEO

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Expression data for program activation by IR-induced DNA breaks in G1 phase Murine PreB cells

Project description:The objective of this set of samples is to identify genes that are differentially expressed following the introduction of DNA double strand breaks (DSBs) by ionizing radiation in wild-type murine pre-B cells. The data generated in this project will be compared to the data generated in GSE9024, in which genes that are differentially expressed following the introduction of DNA double strand breaks (DSBs) by the Rag proteins in murine pre-B cells were examined. In order to understand the differences between the physiologic and genotoxic responses to DSB DNA damage, we need to compare cells that are all in the same compartment of the cell cycle. We are therefore examining the response to IR-induced damage in cells that are arrested in G1, which would correspond to our previous study of G1 arrested cells with Rag-induced breaks. This will illuminate the difference directly, allowing us to better understand the signaling responses to the different types of DNA damage. Murine v-abl-transformed pre-B cells were treated with 3 uM STI571 for 48 hours. The cell type is Wild type (3 biological replicates). For each wild type cell line, cells were treated with 1 Gy ionizing radiation or no ionizing radiation. Each sample was hybridized once using Affymetrix Mouse Genome 2.0 GeneChip arrays (Mouse 430 v2, Affymetrix, Santa Clara, CA). Data were analyzed using the unirradiated samples as the controls.

2013-03-13 | E-GEOD-36530 | biostudies-arrayexpress

Gene activation by Rag-mediated DNA double-strand breaks in G1-phase murine pre-B cells

Project description:The objective is to identify genes that are differentially expressed following the introduction of DNA double-strand breaks (DSBs) by the Rag proteins in murine pre-B cells. Cells lacking Artemis are used since the Rag-induced DSBs will not be repaired, and thus, will provide a continuous stimulus to the cell. Murine v-abl-transformed pre-B cells were treated with 3 uM STI571 for 48 hours. Cell types included RAG-2-deficient (3 biological replicates) and Artemis-deficient (3 biological replicates) G1-phase pre-B cells. Each sample was hybridized once using Affymetrix Mouse Genome 2.0 GeneChip arrays (Mouse 430 v2, Affymetrix, Santa Clara, CA). Data were analyzed using the RAG-2-deficient samples as the controls.

2013-03-13 | E-GEOD-38044 | biostudies-arrayexpress

Gene activation by Rag-mediated DNA double-strand breaks in G1-phase murine pre-B cells

2013-03-13 | GSE38044 | GEO

Chromosomal translocations are guided by the spatial organization of the genome

Project description:The extent to which the three-dimensional organization of the genome contributes to chromosomal translocations is an important question in cancer genomics. We now have generated a high-resolution Hi-C spatial organization map of the G1-arrested mouse pro-B cell genome and mapped translocations from target DNA double-strand breaks (DSBs) within it via high-throughput genome-wide translocation sequencing. RAG endonuclease-cleaved antigen-receptor loci are dominant translocation partners for target DSBs regardless of genomic position, reflecting high frequency DSBs at these loci and their co-localization in a fraction of cells. To directly assess spatial proximity contributions, we normalized genomic DSBs via ionizing-radiation. Under these conditions, translocations were highly enriched in cis along single chromosomes containing target DSBs and within other chromosomes and sub-chromosomal domains in a manner directly related to pre-existing spatial proximity. Our studies reveal the power of combining two high-throughput genomic methods to address long-standing questions in cancer biology. Hi-C interaction maps for WT and ATM -/- G1-arrested AMuLV-transformed pro-B cell lines.

2012-02-16 | E-GEOD-35519 | biostudies-arrayexpress

Cell cycle-dependent resolution of DNA double-strand breaks repair

Project description:Damage to genomic DNA, especially as DNA double strand breaks (DSB), elicits prompt activation of DNA damage response (DDR) which arrest cell-cycle either G1/S or G2/M to avoid entering S and M phase with DNA damage. In mammalian organs cells are in both proliferating and quiescent states. Quiescent cells are already arrested in G0, therefore there may be fundamental difference in DDR between proliferating and quiescent cells. To address these differences we studied recruitment of DSB repair factors and resolution of DNA lesions induced at site-specific DSBs occurring at different cell cycle phases, i.e. in asynchronously proliferating, G0, and G1 arrested cells. Strikingly, DSBs occurring in G0 quiescent cells are irreparable with a sustained activation of p53-pathway. Conversely, reentry of G0-damaged cells into cell cycle progression, show a delayed clearance of recruited DNA repair factors bound at DSBs, indicating an inefficient repair when compared to DSBs induced in asynchronously proliferating or G1 cells. Moreover, we found that initial recognition of DSBs and assembly of DSB factors is largely similar at different cell cycle phases. Our study thereby demonstrates the crucial role of cell cycle phases in repair and resolution of DSBs.

2015-12-30 | GSE71447 | GEO

Genome-wide mapping of early replication fragile sites (ERFS)

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

Genome-wide mapping of early replication fragile sites (ERFS)

2013-02-04 | GSE43504 | GEO

Gene activation by Rag-mediated DNA double strand breaks

Project description:The objective is to identify genes that are differentially expressed following the introduction of DNA double strand breaks (DSBs) by the Rag proteins in murine pre-B cells. Cells lacking Artemis are used since the Rag-induced DSBs will not be repaired and, thus, will provide a continuous stimulus to the cell. Cells lacking Artemis and Atm are used to determine which gene expression changes depend on Atm and cells lacking Artemis that express an I kappa B alpha dominant negative are used to determine which gene expression changes depend on NFkB.

2008-10-12 | GSE9024 | GEO

RPA accumulation during class switch recombination represents 5'-3' DNA end resection during the S-G2/M phase of the cell cycle

Project description:AID promotes chromosomal translocations by inducing DNA double-strand breaks (DSBs) at immunoglobulin (Ig) genes and oncogenes in G1. RPA is a ssDNA-binding protein that associates with resected DSBs in the S phase and facilitates the assembly of factors involved in homologous repair (HR) such as Rad51. Notably, RPA deposition also marks sites of AID-mediated damage, but its role in Ig gene recombination remains unclear. Here we demonstrate that RPA associates asymmetrically with resected ssDNA in response to lesions created by AID, RAG, or other nucleases. Small amounts of RPA are deposited at AID targets in G1 in an ATM-dependent manner. In contrast, recruitment in S-G2/M is extensive, ATM-independent, and associated with Rad51 accumulation. RPA in S-G2/M increases in NHEJ-deficient lymphocytes, where there is more extensive DNA-end resection. Thus, most RPA recruitment during CSR represents salvage of un-repaired breaks by homology-based pathways during the S-G2/M phases of the cell cycle. Chip-Seq of RPA from mouse activated B cells (n = 40), mouse thymocytes (n = 6), and MEFs (n = 1). Different genotypes and/or inhibitors were used.

2013-01-02 | E-GEOD-42451 | biostudies-arrayexpress

RPA accumulation during class switch recombination represents 5'-3' DNA end resection during the S-G2/M phase of the cell cycle

2013-01-02 | GSE42451 | GEO

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