The centralspindlin complex regulates cytokinesis and morphogenesis in the C. elegans spermatheca

Organ morphogenesis needs orchestration of a series of cellular events, including cell division, cell shape change, cell rearrangement and cell death. Cytokinesis, the final step of cell division, is involved in the control of organ size, shape and function. Mechanistically, it is unclear how the molecules involved in cytokinesis regulate organ size and shape. Here, we demonstrate that the centralspindlin complex coordinates cell division and epithelial morphogenesis by regulating cytokinesis. Loss of the centralspindlin components CYK-4 and ZEN-4 disrupts cell division, resulting in altered cell arrangement and malformation of the Caenorhabditis elegans spermatheca. Further investigation revealed that most spermathecal cells undergo nuclear division without completion of cytokinesis. Germline mutant -based analyses suggest that CYK-4 regulates cytokinesis of spermathecal cells in a GTPase activator activity-independent manner. Spermathecal morphology defects can be enhanced by double knockdown of rho-1 and cyk-4, and partially suppressed by double knockdown of cdc-42 and cyk-4. Thus, the centralspindlin components CYK-4 and ZEN-4, together with RHO-1 and CDC-42, are central players of a signaling network that guides spermathecal morphogenesis by enabling completion of cytokinesis.

Automated summary

Organ morphogenesis requires coordination of cellular events, including cell division, shape change, rearrangement, and death. However, the regulatory mechanism of cytokinesis in organ size and shape remains unclear. This study demonstrates that the centralspindlin complex regulates cytokinesis and epithelial morphogenesis, affecting cell division and causing malformation in Caenorhabditis elegans spermatheca. Analysis shows that CYK-4 regulates cytokinesis of spermathecal cells in a GTPase activator activity-independent manner. Furthermore, the centralspindlin components CYK-4 and ZEN-4, along with RHO-1 and CDC-42, play crucial roles in a signaling network that guides spermathecal morphogenesis by enabling completion of cytokinesis.