Loss of a p53-associated G1 checkpoint does not decrease cell survival following DNA damage.

Published

Journal Article

Cell cycle checkpoints regulate progression through the cell cycle. In yeast, loss of the G2 checkpoint by mutation of the rad9 gene results in increased genetic instability as well as increased sensitivity to ionizing radiation. In contrast, comparing clonogenic survival of cells which are isogeneic except for p53 functional status, we find that loss of a G1 checkpoint in mammalian cells is not associated with increased sensitivity to the lethal effects of ionizing radiation or a topoisomerase I inhibitor, camptothecin. These results indicate that increased sensitivity to DNA-damaging agents is not necessarily a defining feature of a mammalian cell cycle checkpoint. Furthermore, in light of a recent link of p53 function to radiation-induced apoptosis in hematopoietic cells, these observations suggest that p53-dependent apoptosis is a cell type-specific phenomenon and thus predict that the biological consequences of loss of p53 function will be cell type specific.

Full Text

Duke Authors

Cited Authors

  • Slichenmyer, WJ; Nelson, WG; Slebos, RJ; Kastan, MB

Published Date

  • September 1, 1993

Published In

Volume / Issue

  • 53 / 18

Start / End Page

  • 4164 - 4168

PubMed ID

  • 8364909

Pubmed Central ID

  • 8364909

Electronic International Standard Serial Number (EISSN)

  • 1538-7445

International Standard Serial Number (ISSN)

  • 0008-5472

Language

  • eng