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CP110 suppress a cilia assembly program.  Mammalian centrioles
play a dynamic role in centrosome function, but they also have
the capacity to nucleate the assembly of cilia. Although
controls must exist to specify these different fates, the key
regulators remain largely undefined. We have purified complexes
associated with CP110, a protein that plays an essential role in
centrosome duplication and cytokinesis, and have identified a
previously uncharacterized protein, Cep97, that recruits CP110
to centrosomes. Depletion of Cep97 or expression of dominant-
negative mutants results in CP110 disappearance from
centrosomes, spindle defects, and polyploidy. Remarkably, loss
of Cep97 or CP110 promotes primary cilia formation in growing
cells, and enforced expression of CP110 in quiescent cells
suppresses their ability to assemble cilia, suggesting that
Cep97 and CP110 collaborate to inhibit a ciliogenesis program.
Identification of Cep97 and other genes inv