Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Transcription profiling of lung tissue from transcription-coupled repair-deficient (Csb-/-) and wild type mice in response to ozone

ABSTRACT: We investigated whether transcription-coupled repair deficient mice (Cockayne syndrome B knockout mice (Csb-/-)), known to be sensitive to oxidative stressors, have a different response to ozone than its repair-proficient control, Csb heterozygote (Csb+/-) mice.

ORGANISM(S): Mus musculus

SUBMITTER: Ingeborg Kooter

PROVIDER: E-TABM-137 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Ozone induces clear cellular and molecular responses in the mouse lung independently of the transcription-coupled repair status.

Kooter Ingeborg M IM Pennings Jeroen L A JL Fokkens Paul H B PH Leseman Daan L A C DL Boere A John F AJ Gerlofs-Nijland Miriam E ME Cassee Flemming R FR Schalk Johanna A C JA Orzechowski Tom J H TJ Schaap Mirjam M MM Breit Timo M TM Dormans Jan A M A JA van Oostrom Conny T M CT de Vries Annemieke A van Steeg Harry H

Journal of applied physiology (Bethesda, Md. : 1985) 20061109 3

The oxidant ozone is a well-known air pollutant, inhalation of which is associated with respiratory tract inflammation and functional alterations of the lung. It is well established as an inducer of intracellular oxidative stress. We investigated whether Cockayne syndrome B, transcription-coupled, repair-deficient mice (Csb(-/-)), known to be sensitive to oxidative stressors, respond differently to ozone than repair-proficient controls (Csb(+/-)). Mice were exposed to 0.8 parts/million ozone for ...[more]

PMID: 17095637

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Project description:Cockayne syndrome is an inherited premature aging syndrome associated with developmental and neurological disorders. Mutations in the genomic locus encoding CSB are associated with 80% Cockayne syndrome cases. Transcription profiling assays reveal the association of mis-regulation of gene expression with Cockayne syndrome, highlighting the importance of CSB in transcription regulation. However, many questions remain unanswered as how CSB regulates transcription. In this study, we dissect the mechanisms by which CSB regulates transcription during normal growth. By anti-CSB chromatin immunoprecipitation followed by deep sequencing, we found CSB is enriched at genomic regions containing TGASTCA motifs, to which the immediate early gene product C-Jun binds specifically. We further demonstrate that c-Jun co-immunoprecipitates with CSB. In addition, the targeting of CSB to genomic region containing TGASTCA motifs was drastically reduced in cells treated c-Jun shRNA. Reverse transcription followed by quantitative PCR indicates that CSB can regulate gene expression nearby its binding sites, both in activation and repression. The remodeling defective CSBM-bM-^HM-^FN1 mutant is also targeted to TGASTCA motifs, but cannot always substitute CSB function in transcription regulating, suggesting the importance of remodeling by CSB in transcription regulation. Notably, the Cockayne syndrome related mutation encoding protein CSBR670W, which is defective in ATP hydrolysis but is targeted to TGASTCA motifs efficiently, indicating that ATP hydrolysis is dispensable for c-Jun mediated CSB targeting, in sharp contrast to the ATP-dependent targeting mechanism by which CSB is relocated to DNA lesion stalled transcription. Together, these results reveal a second CSB targeting mechanism in which DNA sequence specific transcription factor c-Jun targets CSB to specific genomic region and regulate gene expression. Genomic localization of CSB and remodeling deficient CSBM-bM-^HM-^FN1

Dataset Information

Transcription profiling of lung tissue from transcription-coupled repair-deficient (Csb-/-) and wild type mice in response to ozone

Publications

Ozone induces clear cellular and molecular responses in the mouse lung independently of the transcription-coupled repair status.

Similar Datasets

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