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Mol Cell Biol. 2011 Apr;31(7):1470-7. doi: 10.1128/MCB.01330-10. Epub 2011 Jan 24.

Early-onset aging and defective DNA damage response in Cdc14b-deficient mice.

Author information

  • 1Department of Molecular Physiology and Biophysics, BCM335, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.

Abstract

The Cdc14 dual-specificity phosphatase plays a key role in the mitotic exit of budding yeast cells. Mammals have two homologues, Cdc14a and Cdc14b. Unlike the yeast counterpart, neither Cdc14a nor Cdc14b seems to be essential for mitotic exit. To determine the physiological function of Cdc14b, we generated mice deficient in the phosphatase. The mutant mice were viable and did not display overt abnormalities. However, these mice developed signs of aging at much younger ages than the wild-type mice. At the cellular level, the Cdc14b-deficient mouse embryonic fibroblasts (MEFs) grew more slowly than the controls at later passages as a result of increased rates of senescence. Consistent with these premature-aging phenotypes, Cdc14b-deficient cells accumulated more endogenous DNA damage than the wild-type cells, and more Cdc14b-deficient MEFs entered senescence than control MEFs in response to exogenous DNA damage. However, no deficiencies in DNA damage checkpoint response were detected in Cdc14b mutant cells, suggesting that the function of Cdc14b is required for efficient DNA damage repair.

PMID:
21262768
[PubMed - indexed for MEDLINE]
PMCID:
PMC3135283
Free PMC Article

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