In the cytoplasm, a common pool of actin monomers (G-actin) competes for the different co-existing actin-based networks, but it is unclear how this homeostatic balance is regulated, in particular with regard to the mechanisms that contribute to F-actin disassembly. Oocytes are a valuable system to address this question as they experience a major remodelling of their actin cytoskeleton in meiosis, and in this work (Bourdais et al., 2021), Guillaume Halet and co-workers explore the role of the actin-depolymerising factor cofilin during meiotic progression. They found that, unexpectedly, cofilin is phosphorylated and thus inactivated during prophase arrest and becomes active at meiosis resumption. Furthermore, inhibition of cofilin during meiosis-I, induced by overexpressing its inactivating kinase, results in an elongation of microvilli and a reciprocal depletion of cytoplasmic F-actin, giving rise to cytokinesis defects. In contrast, when cofilin is inactivated during meiosis-II, the turnover of actin filament networks ceases and a dramatic overgrowth of the polarised actin cap is observed. These findings clearly establish a role for cofilin in actin network homeostasis in meiosis, in line with cell cycle progression. Furthermore, the authors propose that oocyte microvilli act as a sink for actin monomers to balance competing cytoplasmic and cortical actin networks, and it will be interesting to investigate whether a similar regulation also exists in other cells with microvilli.
