Cofilin regulates actin network homeostasis and microvilli length in mouse oocytes

Abstract

How multiple actin networks coexist in a common cytoplasm, while competing for a shared pool of monomers, is still an ongoing question. This is exemplified by meiotic maturation in the mouse oocyte, which relies on the dynamic remodeling of distinct cortical and cytoplasmic F-actin networks. Here we show that the conserved actin-depolymerizing factor cofilin is activated in a switch-like manner at meiosis resumption from prophase arrest. Interfering with cofilin activation during maturation resulted in widespread microvilli elongation, while cytoplasmic F-actin was depleted, leading to defects in spindle migration and polar body extrusion. In contrast, cofilin inactivation in metaphase II-arrested oocytes resulted in a shutdown of F-actin dynamics, along with a dramatic overgrowth of the polarized actin cap. However, inhibition of the Arp2/3 complex to promote actin cap disassembly elicited ectopic microvilli outgrowth in the polarized cortex. These data establish cofilin as a key player in actin network homeostasis in oocytes, and reveal that microvilli can act as a sink for monomers upon disassembly of a competing network.

Plasma membrane topography governs the three-dimensional dynamic localization of IgM B cell receptor clusters

“…We further speculate that MV elongation may be regulated by external signals warning B cells of an infection or by soluble factors from specialized antigen-bearing cells. This is in line with the finding that TLR4 signaling increases IgM-BCR mobility and promotes cofilin activity, a molecule involved in MV elongation [46,47]. Movement of IgM-BCR clusters from MV roots towards the MT could further function to reduce the threshold for BCR activation, as the transmembrane phosphatase CD45 that negatively regulates BCR activation has been found to be excluded from MT [36].…”

Mild Photothermal Therapy Prevents Posterior Capsule Opacification through Cytoskeletal Remodeling

“…The transduction of the YAP between cytoplasm and nucleus modulated F‐actin polymerization and stress fiber formation. [ 47 ] Overall, the reduced expression of the p‐cofilin, p‐ERM, and p‐YAP disrupted the actin cytoskeleton and controlled structural arrangement.…”

Intercellular communication in the cumulus–oocyte complex during folliculogenesis: A review

“…Estrogen could also regulate the expression of alpha-actinin and the localization of ezrin-phosphate and SLC9A3R1 on the oocyte membrane, which is required for microvilli development. Bourdais et al ( Bourdais et al, 2021 ). Proposed that cofilin played a key role in oocyte actin network homeostasis and microvilli regulation.…”