page 807 indicate that this migration is dependent on a Rho-associated kinase in a process that may link two distinct events in cytokinesis.
Both the mother and daughter centrosomes are made up of a centriole and the surrounding pericentriolar matrix (PCM). The mother centriole is normally rather immobile, remaining near the cell center throughout most of the cell cycle. In late telophase, however, the mother centriole migrates to the cytoplasmic bridge tethering the daughter cells, signaling the end of mitosis and separation of the cells. Upon exit from mitosis, the mother centriole again returns to a nearly immobile state near the cell center.
This behavior of the mother centriole at the end of mitosis is dependent on a Rho-associated kinase, p160ROCK, which Chevrier et al. found at the PCM of the mother centriole. Premature migration toward the midbody could be initiated by interference with p160ROCK, indicating that this activity suppresses mother centriole movement. This effect is actin independent, but microtubule dependent. Possibly, p160ROCK prevents asymmetric microtubule organization required to direct mother centriole migration to the midbody.
p160ROCK also acts on the centrosome itself to keep the two centrioles together. During S and G2 phases, mother and daughter centrioles are normally found in close proximity. Inhibition of p160ROCK activity resulted in wider than normal separation of the two centrioles in these phases. p160ROCK was found in a linking structure between the two centrioles. Thus, the down-regulation of Rho, which is known to occur in late telophase, may lead to relaxation of this tether by inhibiting p160ROCK. This would allow the centrioles to separate and the mother centriole to migrate to the midbody. In the future, the group hopes to identify substrates of the kinase at the centrosome. ▪