Journal Article

The relationship between <i>p53</i> status, DNA repair and chromatid aberration induction in G<sub>2</sub> mouse embryo fibroblast cells treated with bleomycin

E.Maria Donner and R.Julian Preston

in Carcinogenesis

Volume 17, issue 5, pages 1161-1165
Published in print May 1996 | ISSN: 0143-3334
e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/17.5.1161
The relationship between p53 status, DNA repair and chromatid aberration induction in G2 mouse embryo fibroblast cells treated with bleomycin

More Like This

Show all results sharing this subject:

  • Clinical Cytogenetics and Molecular Genetics

GO

Show Summary Details

Preview

The involvement of p53 in the formation of chromosome aberrations was assessed by analyzing bleomycin-induced, chromatid-type aberrations in G2 phase fibroblasts derived from embryos from wild-type and p53 knock-out mice. Cells that were p53 +/− or p53−/− were more sensitive to the induction of aberrations than the p53+/+cells, particularly at concentrations of 7.5 and 10.0 llg/ml. The p53-deficient cells also showed an overdispersed distribution of bleomycin-induced chromatid aberrations, a greater amount of overall genomic instability and a possible loss of a cell death pathway. These data are interpreted as indicating a role for p53 in DNA repair in the G2 phase, with a loss of p53 leading to an increased frequency of deletions (incomplete repair) and interchanges (misrepair). The specific role remains to be elucidated. The mitotk index decreased with increasing bleomycin concentration to a similar extent in all three cell lines, indicating that the loss of a G2 checkpoint in p53−/− and p53+/− cells was not an explanation for the increased sensitivities in these cells compared with the p53+/+.

Journal Article.  0 words. 

Subjects: Clinical Cytogenetics and Molecular Genetics

Full text: subscription required

How to subscribe Recommend to my Librarian

Users without a subscription are not able to see the full content. Please, subscribe or login to access all content.