Regulation of actomyosin contractility in C. elegans
Ronen Zaidel-Bar, Mechanobiology Institute Singapore and Tel-Aviv University Medical School
The actomyosin cortex is responsible for cell shape and for dynamic processes such as cell polarization and cytokinesis. We are studying the regulation of cortical contractility in the C. elegans zygote, using genetic loss of function and live-imaging. In my talk, I will discuss recent findings regarding two proteins: the actin cross-linking protein plastin (PLST-1) and the transmembrane receptor E-cadherin (HMR-1). Consistent with previous in-vitro reconstitution studies, we show that an optimal level of cross-linking by plastin is required for the generation of coordinated long-range contractions in the cortex; without the connectivity afforded by plastin, zygote polarization and cytokinesis are severely perturbed. E-cadherin is well known for its role as a cell-cell adhesion receptor.
Surprisingly, we discovered a role for non-junctional E-cadherin clusters in regulating cortical contractility. E-cadherin clusters inhibit RhoA and non-muscle myosin II activity at the cortex and form a physical barrier that slows actin flows. In the absence of non-junctional E-cadherin cytokinesis proceeds faster, but the cortex is also at a risk of detaching from the plasma membrane. Thus, our studies in the C. elegans zygote are shedding light on structural and regulatory mechanisms underlying cortex function.