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Unknown,Transcriptomics,Genomics,Proteomics

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DNA damage responses activate a multi-functional genetic program in murine bone marrow-derived macrophages

ABSTRACT: DNA damage response kinase ATM regulates the genetic program of lymphocytes with phsiologically induced DNA DSBs. In bone marrow-derived macrophages, related kinase DNAPKcs is also responsible for activating DNA damage responses after infection with Listeria monocytogenes. Here we show that both ATM and DNA-PKcs regulate the genetic program of Listeria monocytogenes-infected macrophages. Two independent bone marrow-derived macrophage cultures for each genotype (LysMcre/+ and Scid: Atmc/c: LysMcre/+) were infected with Listeria monocytogenes for 24 hrs at an MOI of 5. RNA was isolated using RNeasy (Qiagen). Gene expression profiling was performed using Illumina MouseRef-8 expression microarrays.

ORGANISM(S): Mus musculus

SUBMITTER: Barry Sleckman

PROVIDER: E-GEOD-70467 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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DNA damage responses activate a multi-functional genetic program in murine bone marrow-derived macrophages

Project description:DNA damage response kinase ATM regulates the genetic program of lymphocytes with phsiologically induced DNA DSBs. In bone marrow-derived macrophages, related kinase DNAPKcs is also responsible for activating DNA damage responses after infection with Listeria monocytogenes. Here we show that both ATM and DNA-PKcs regulate the genetic program of Listeria monocytogenes-infected macrophages.

2015-07-03 | GSE70467 | GEO

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2011-12-02 | E-GEOD-34083 | biostudies-arrayexpress

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2016-01-26 | E-MTAB-3598 | biostudies-arrayexpress

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2017-06-30 | E-MTAB-5784 | biostudies-arrayexpress

Transcription profiling of mouse bone marrow derived macrophages

Project description:Macrophages phagocytose bacteria. Certain pathogenic bacteria access and replicate within the cytosol of infected macrophages and induce changes in macrophage gene expression by triggering of innate immune receptors and/or the effects of bacterial virulence factors. We used microarray analysis to identify changes in macrophage gene expression following infection with Listeria monocytogenes. Experiment Overall Design: Macrophages were cultured from bone marrow of female C57BL/6 mice using 10% L-cell conditioned media and mock infected (3 chips) or infected with log phase L. monocytogenes (2 chips). Samples were harvested for RNA isolation at 10 h after infection. Experiment Overall Design: Supplementary file below reports Genesifter-processed data: mean ("P" only) signal intensities and SEM for the MOCK and LM_INF groups.

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Misregulation of the broad-range phospholipase C activity increases the susceptibility of Listeria monocytogenes to intracellular killing by neutrophils

Project description:Listeria monocytogenes is a facultative intracellular bacterial pathogen that tightly regulates the activities of various virulence factors during infection. A mutant strain (the plcBM-NM-^Tpro mutant) that has lost the ability to control the activity of a phospholipase C (PC-PLC) is attenuated a hundred fold in mice. This attenuation is not due to a lack of bacterial fitness, but appears to result from a modified host response to infection. The transcriptomic pattern of immunerelated genes in infected macrophages indicated no differential response to wild-type L. monocytogenes vs the plcBM-NM-^Tpro mutant. Cultures of bone marrow derived macrophages from BALB/c were infected with either wild type or mutant L. monocytogens for 3, 6, or 9 hrs. The macrophages were then collected and RNA isolated for microarray analysis of gene expression.

2013-08-14 | E-GEOD-49820 | biostudies-arrayexpress

Contribution of the STAT1alpha and STAT1beta isoforms to IFN-gamma mediated innate immunity

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2014-04-04 | E-GEOD-48970 | biostudies-arrayexpress

TLR signalling induced by bacterial RNA vs R848

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2012-05-08 | E-MTAB-1139 | biostudies-arrayexpress

Phosphorylation of DNA-PKcs at the S2056 cluster ensures efficient and productive lymphocyte development in XLF-deficient mice

Project description:The non-homologous end-joining (NHEJ) pathway is a major DNA double-strand break repair pathway in mammals and is essential for lymphocyte development. Ku70 and Ku80 heterodimer (KU) initiates NHEJ, thereby recruiting and activating the catalytic subunit of DNA-dependent protein kinase (DNA-PKcs). While DNA-PKcs deletion only moderately impairs end-ligation, the expression of Kinase-dead DNA-PKcs completely abrogates NHEJ. Active DNA-PK phosphorylates DNA-PKcs at two clusters – PQR around S2056 (S2053 in mouse) and ABCDE around T2609. Alanine substitution at the S2056 cluster moderately compromises end-ligation on plasmid-based assays. But mice carrying alanine substitution at all 5 serine residues within the S2056 cluster (DNA-PKcsPQR/PQR) display no defect in lymphocyte development, leaving the physiological significance of S2056 cluster phosphorylation elusive. XLF is a non-essential NHEJ factor. Xlf-/- mice have substantial peripheral lymphocytes that are completely abolished by the loss of DNA-PKcs, the related ATM kinases, other chromatin associated DNA damage response factors (e.g., 53BP1, MDC1, H2AX, MRI, etc.) or RAG2-C-terminal regions, suggesting functional redundancy. While ATM inhibition does not further compromise end-ligation, here we show that in XLF-deficient background, DNA-PKcs S2056 cluster phosphorylation is critical for normal lymphocyte development. Chromosomal V(D)J recombination from DNA-PKcsPQR/PQRXlf-/- B cells is efficient but often has large deletions that jeopardize lymphocyte development. Class switch recombination junctions from DNA-PKcsPQR/PQRXlf-/- mice are less efficient and the residual junctions display decreased fidelity and increased deletion. These findings establish a role for DNA-PKcs S2056 cluster phosphorylation in physiological chromosomal NHEJ, implying that S2056 cluster phosphorylation contributes to the synergy between XLF and DNA-PKcs in end-ligation.

2023-05-01 | GSE228850 | GEO

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