Cdc14B depletion leads to centriole amplification, and its overexpression prevents unscheduled centriole duplication

Jun Wu, Hyekyung P. Cho, David B. Rhee, Dabney K. Johnson, John Dunlap, Yie Liu, Yisong Wang

Research output: Contribution to journalArticle

39 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)475-483
Number of pages9
JournalJournal of Cell Biology
Volume181
Issue number3
DOIs
StatePublished - May 5 2008

ASJC Scopus subject areas

  • Cell Biology

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