Anillin mediates unilateral furrowing during cytokinesis by limiting RhoA binding to its effectors.

Abstract

During unilateral furrow ingression, one side of the cytokinetic ring (leading edge) ingresses before the opposite side (lagging edge). Anillin mediates unilateral furrowing during cytokinesis in the one-cell C. elegans zygote by limiting myosin II accumulation in the ring. Here, we address the role of anillin in this process and show that anillin inhibits not only the accumulation of myosin II but also of other RhoA effectors by binding and blocking the RhoA effector site. The interaction between the anillin's RhoA-binding domain (RBD) and active RhoA is enhanced by the disordered linker region and differentially regulated at the leading and lagging edge, which together results in asymmetric RhoA signaling and accumulation of myosin II. In summary, we discover a RhoA GEF- and GAP-independent mechanism, where RhoA activity is limited by anillin binding to the RhoA effector site. Spatial fine-tuning of anillin's inhibitory role on RhoA signaling enables unilateral furrow ingression and contributes to animal development.