CP110, a cell cycle-dependent CDK substrate, regulates centrosome duplication in human cells.

Centrosome duplication and separation are linked inextricably to certain cell cycle events, in particular activation of cyclin-dependent kinases (CDKs). However, relatively few CDK targets driving these events have been uncovered. Here, we have performed a screen for CDK substrates and have isolated a target, CP110, which is phosphorylated by CDKs ...
in vitro and in vivo. Human CP110 localizes to centrosomes. Its expression is strongly induced at the G1-to-S phase transition, coincident with the initiation of centrosome duplication. RNAi-mediated depletion of CP110 indicates that this protein plays an essential role in centrosome duplication. Long-term disruption of CP110 phosphorylation leads to unscheduled centrosome separation and overt polyploidy. Our data suggest that CP110 is a physiological centrosomal CDK target that promotes centrosome duplication, and its deregulation may contribute to genomic instability.
Mesh Terms:
Amino Acid Motifs, Amino Acid Sequence, Cell Cycle Proteins, Centrosome, Cloning, Molecular, Cyclin-Dependent Kinases, DNA, Complementary, G1 Phase, Gene Expression Regulation, HeLa Cells, Humans, In Situ Hybridization, Fluorescence, Microtubule-Associated Proteins, Molecular Sequence Data, Mutagenesis, Site-Directed, Phosphoproteins, Phosphorylation, Polyploidy, RNA, Small Interfering, Recombinant Proteins, S Phase, Sensitivity and Specificity, Sequence Alignment, Substrate Specificity, Tumor Cells, Cultured
Dev. Cell
Date: Sep. 01, 2002
Download Curated Data For This Publication
Switch View:
  • Interactions 9