The RhoGEF ECT-2 is required for ventral enclosure during C. elegans embryogenesis

摘要: Tissue morphogenesis is crucial for the development of metazoans. C. elegans, a model system studying tissue morphogenesis, as there are many genetic tools available, and embryos amenable to microscopy. We study ventral enclosure, which process where epidermal cells migrate enclose elegans embryo in single layer cells. This initiated by migration adhesion two pairs anterior leading cells, followed eight posterior pocket The mediated F-actin rich filopodia-like protrusions, under control Rac – Wave/Scar Arp2/3 pathway. Cables become enriched around margins form ring, early studies showed that this ring tension. Based on data, actomyosin contractility was predicted mediate closure during enclosure. However, nonmuscle myosin has not been studied it could regulate addition regulating cell shape changes and/or adhesion. For example, proteins junction complexes also required they maintain contacts between so can unit new junctions with contralateral neighbors. Our support role RhoA regulates cytokinesis elongation lateral late embryogenesis. ECT-2 GEF activates cytokinesis, different GEF, RHGF-2, A hypomorphic, maternal ts allele ect-2, ax751, polarity embryo, but displays few defects, especially at non-permissive temperatures. Using allele, we found ect-2 neuroblasts earlier embryonic stages, Genetic crosses suggest functions parallel pathway may be part Rho contractility, supporting Imaging quantification expressing GFP-tagged forms into supracellular structure reminiscent actin described previously. enrichment organization myosin, requirement contractility. Interestingly, function cadherin/catenin junctions, suggesting filaments contribute