Closing while flowing: How a shrinking cytokinetic interface avoids membrane self-congestion

Animal cytokinesis is often described as constriction of a RhoA-dependent actomyosin contractile ring. Yet, this ring operates within a shrinking membrane-cortex interface into which cortical flow continually delivers mechanically engaged material, creating a mass-balance problem: how can the interface close without becoming congested? Here, I propose a membrane-centric framework in which sustained furrow ingression depends on coordinated Loading and Relief. Actomyosin contractility gathers and compresses membrane-cortex material at the furrow apex, while membrane-proximal, RhoA-dependent anillo-septin assemblies are proposed to facilitate slip-mediated Lateral Relief by routing material away from the contractile ring proper. The ring remains central, but within a wider three-dimensional cleavage zone where cortical lamination allows inflow and outflow to occur simultaneously. This framework predicts that furrow progression and robustness depend on efficient redistribution of membrane-cortex material, while geometrical advance need not directly report material-processing rate. It suggests direct tests of whether impaired disengagement and exit cause material retention, altered furrow dynamics, and congestion.