The role of cell signalling and cortical polarity on cytokinesis in C. elegans.

Abstract

The molecular requirements for cytokinesis, the final stage of cell division, differ based on cell
identity and the external environment. Knockdown of cytoskeletal components in Drosophila,
mouse, and C. elegans causes cell-specific cytokinesis failure. Furthermore, some cells naturally
undergo cytokinesis failure to generate binucleate or polyploid cells. The formin, CYK-1, is required to nucleate unbranched actin filaments to form the contractile ring during cytokinesis.
However, while inactivation of this formin in the C. elegans four-cell embryo causes consistent
division failure in the two AB cells, some EMS and P2 cells successfully divide. Division in EMS
under these weakened conditions is dependent on contact with P2, suggesting that signals from P2
protect cytokinesis in EMS. We have carried out an RNAi screen that has identified components
of the Wnt and Src signalling pathways that are important for division in EMS when CYK-1 is
inactivated. Knockdown of Wnt signalling causes changes in actomyosin distribution and reduced
cortical pulling force, but the abundance of major contractile ring components are not changed. We
have also developed a system allowing cell-specific knockdown of CYK-1 in seam cells (a larval cell
type), using the auxin-inducible degron system. Seam cells are highly resistant to CYK-1 depletion
and the rate of cell division failure under these weakened conditions is also cell-specific. Together,
these results demonstrate that the requirement for CYK-1 for successful cytokinesis varies more
than would be expected, and raises questions about the mechanisms that ensure robust cytokinesis
across cell types when the contractile ring is weakened.