A model for anillin regulation and function during cytokinesis. Pathways controlled by RhoGEFPbl, including well-documented inputs into F-actin and myosin II (black) and a novel, separate input (pink) via anillin and septins (A). Through equatorial stimulation (1), MTs spatially control Rho activation and the independent recruitment of Dia, Rok, and anillin to the equatorial cortex. F-actin and Rok/myosin II contribute to equatorial focusing of anillin (and other cortical components) via cortical flow (2), whereas Rho–anillin–Septin complexes dynamically link contractile elements within the furrow to the plasma membrane (PM) and to MT plus ends, thus preventing the lateral instability of the furrow seen upon anillin RNAi. (B) LatA may stabilize Rho–anillin–Septin complexes by preventing their normal F-actin–dependent disassembly (A, blue). Continued assembly with blocked disassembly gives rise to the filamentous structures in LatA, perhaps mimicking midbody biogenesis that normally accompanies local loss of F-actin at the close of furrowing.
