Polarization fails when centrosomal components are removed (left) but proceeds in the absence of microtubule nucleation (right).


The C. elegans embryo lacks polarity until ∼30 min after fertilization. Prior evidence implicated the sperm-donated centrosome, presumably via its ability to nucleate microtubules, in polarity establishment. Now, Carrie Cowan and Anthony Hyman (Max Planck Institute, Dresden, Germany) find that it is centrosomes themselves that are needed. When they ablate the centrosome, downstream polarity signals such as PAR proteins fail to localize as they do in wild-type embryos.

Timing of the centrosome's ablation is crucial. When the team knocks out the centrosome before it approaches the cortex of the cell, polarity is abolished. However, if the team ablates the centrosome after it nears the cortex, they induce only slight disruptions in the downstream polarity events. Thus, the required signal is a transient one.

That was unexpected. Dogma in the field was that it was the centrosome's ability to nucleate microtubules that was critical for polarity, as microtubules were thought to transport crucial vesicles or molecules to the cortex. But microtubule nucleation occurs after the critical polarity signal and is now shown not to be needed for polarity establishment. “This is a real signaling event,” says Cowan. “The centrosome appears to be a scaffold for some signaling molecule.”

The German group wants to know what causes the centrosome to move to the cortex and just how close it has to get to start PAR localization. One idea is that the centrosome signal punctures the actin meshwork at the cortex and induces cortical flows, but the identity of a centrosome-based signal that might cause such a break remains a mystery. ▪


Cowan, C.R., and A.A. Hyman.