Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Transcription profiling of wild type, Trp53-null and Trp53-515C/515C (encoding p53R172P) mouse embryo fibroblasts treated with gamma-radiation

ABSTRACT: Trp53-null, Trp53-515C/515C (encoding p53R172P), or wild-type mouse embryo fibroblasts were treated with 6 Gy gamma-radiation and harvested 6 hours later to compare expression profiles of genes regulated by wild-type p53 and p53R172P. Trp53-null cells were included as a negative control.

ORGANISM(S): Mus musculus

SUBMITTER: Juan Barboza

PROVIDER: E-MEXP-917 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

p21 delays tumor onset by preservation of chromosomal stability.

Barboza Juan A JA Liu Geng G Ju Zhenlin Z El-Naggar Adel K AK Lozano Guillermina G

Proceedings of the National Academy of Sciences of the United States of America 20061214 52

The p53 protein suppresses tumorigenesis by initiating cellular functions such as cell cycle arrest and apoptosis in response to DNA damage. A p53 mutant, p53R172P, which is deficient for apoptosis but retains a partial cell cycle arrest function, delays tumor onset in mice. Remarkably, lymphomas arising in Trp53(515C/515C) mice (encoding p53R172P) retain stable genomes. Given the dominant role of p21 in p53 cell cycle control, we crossed Trp53(515C/515C) mice onto a p21-null background to deter ...[more]

PMID: 17170138

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Project description:Plants exhibit a robust transcriptional response to gamma radiation which includes the induction of transcripts required for homologous recombination and the suppression of transcripts that promote cell cycle progression. Various DNA damaging agents induce different spectra of DNA damage as well as M-bM-^@M-^\collateralM-bM-^@M-^] damage to other cellular components and therefore are not expected to provoke identical responses by the cell. Here we study the effects of two different types of ionizing radiation (IR) treatment, HZE (1 GeV Fe26+ high mass, high charge, and high energy relativistic particles) and gamma photons, on the transcriptome of Arabidopsis thaliana seedlings. Both types of IR induce small clusters of radicals that can result in the formation of double strand breaks (DSBs), but HZE also produces linear arrays of extremely clustered damage. We performed these experiments across a range of time points (1.5-24 h after irradiation) in both wild-type plants and in mutants defective in the DSB-sensing protein kinase ATM. The two types of IR exhibit a shared double strand break-repair-related damage response, although they differ slightly in the timing, degree, and ATM-dependence of the response. The ATM-dependent, DNA metabolism-related transcripts of the M-bM-^@M-^\DSB responseM-bM-^@M-^] were also induced by other DNA damaging agents, but were not induced by conventional stresses. Both Gamma and HZE irradiation induced, at 24 h post-irradiation, ATM-dependent transcripts associated with a variety of conventional stresses; these were overrepresented for pathogen response, rather than DNA metabolism. In contrast, only HZE-irradiated plants, at 1.5 h after irradiation, exhibited an additional and very extensive transcriptional response, shared with plants experiencing M-bM-^@M-^\extended night.M-bM-^@M-^] This response was not apparent in gamma-irradiated plants. We treated 5-day-old WT and atm-1 seedlings of Arabidopsis thaliana with 100 Gy of Gamma radiation (over a span of 15 minutes) or 30 Gy of HZE (over a span of approximately 12 minutes). Gamma irradiations were completed at 8:40 am, while HZE irradiations were conducted in two runs (due to space limitations) which were completed at 1:09 and 1:28pm respectively. Gamma treated seedlings were sampled at 10:10 am, 11:40 am, 2:55 pm, 8:40 pm, and 8:40 am. HZE treated seedlings were sampled at 2:39 pm, 4:09 pm, 7:24 pm, 1:09 am, and 1:09 pm. Un-irradiated WT and atm-1 control seedlings were sampled at 10:45 am on Day #1 and 9:15 am on Day #2. There are a total of 22 experimental or control conditions, with two replicates per condition, yielding 44 samples overall.

Dataset Information

Transcription profiling of wild type, Trp53-null and Trp53-515C/515C (encoding p53R172P) mouse embryo fibroblasts treated with gamma-radiation

Publications

p21 delays tumor onset by preservation of chromosomal stability.

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