Abstract
Early morphogenic movements are an important feature of embryonic development in vertebrates. During zebrafish gastrulation, epiboly progression is driven by the coordinated remodeling of the YSL microtubule network and F-actin cables. We recently described the implication of Nrz, an anti-apoptotic Bcl-2 homolog, in the control of the YSL cytoskeleton dynamics. Nrz knock-down induces premature actin-myosin ring formation leading to margin constriction, epiboly arrest and embryo lethality. At the molecular level, the Nrz protein controls the actin-myosin dynamics through IP3R-dependent calcium levels variation. Here, we discuss these novel findings and propose a model in which reversible phosphorylation of the Nrz/IP3R complex modulates the permeability of the IP3R calcium channel and thus may explain the Nrz-dependent control of IP3R opening required for proper epiboly completion.
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