Cdc14B depletion leads to centriole amplification and its overexpression prevents unscheduled centriole duplication
- ORNL
- University of Tennessee, Knoxville (UTK)
- National Institute on Aging, Baltimore
Centrosome duplication is tightly controlled in coordination with DNA replication. The molecular mechanism of centrosome duplication remains unclear. Previous studies found that a fraction of human proline-directed phosphatase Cdc14B associates with centrosomes. However, Cdc14B's involvement in centrosome cycle control has never been explored. Here, we show that depletion of Cdc14B by RNA interference leads to centriole amplification in both HeLa and normal human fibroblast BJ and MRC-5 cells. Induction of Cdc14B expression through a regulatable promoter significantly attenuates centriole amplification in prolonged S-phase arrested cells and proteasome inhibitor Z-L3VS-treated cells. This inhibitory function requires centriole-associated Cdc14B catalytic activity. Together, these results suggest a potential function for Cdc14B phosphatase in maintaining the fidelity of centrosome duplication cycle.
- Research Organization:
- Oak Ridge National Lab. (ORNL), Oak Ridge, TN (United States); Mouse Genetics Research Facility
- Sponsoring Organization:
- USDOE Laboratory Directed Research and Development (LDRD) Program; Work for Others (WFO); USDOE Office of Science (SC)
- DOE Contract Number:
- DE-AC05-00OR22725
- OSTI ID:
- 931193
- Journal Information:
- Journal of Cell Biology, The, Vol. 181, Issue 3; ISSN 0021-9525
- Country of Publication:
- United States
- Language:
- English
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