Loss of a/753-associated Gl Checkpoint Does Not Decrease Cell Survival following DNA Damage

William J. Slichenmyer, William G. Nelson, Robbert J. Slebos, Michael B. Kastan

Research output: Contribution to journalArticle

Abstract

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, camp-tothecin. These results indicate that increased sensitivity to DNA-damag-ing 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.

Original languageEnglish (US)
Pages (from-to)4164-4168
Number of pages5
JournalCancer Research
Volume53
Issue number18
StatePublished - Sep 1993

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ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

Slichenmyer, W. J., Nelson, W. G., Slebos, R. J., & Kastan, M. B. (1993). Loss of a/753-associated Gl Checkpoint Does Not Decrease Cell Survival following DNA Damage. Cancer Research, 53(18), 4164-4168.