The Dynein-Dynactin complex influences amnioserosa cell morphodynamics and adhesion during Drosophila dorsal closure

Abstract

The contraction of the amnioserosa, which provides the major force for Drosophila dorsal closure, is powered by apical constriction. While much work has demonstrated the requirement for the spatiotemporal regulation of intracellular forces generated by the actomyosin cytoskeleton in patterning apical constriction, the role of the microtubule cytoskeleton remains poorly understood. We previously uncovered the necessity of apical microtubule meshwork reorganisation in patterning apical constriction dynamics, and demonstrated its reliance on EB1-dependent microtubule growth and Patronin-dependent non-centrosomal nucleation. Here we discover the requirement for Dynein-Dynactin complex functions in patterning cell morphodynamics in the amnioserosa. We show that perturbing this complex in multiple ways, including the use of a mutant that likely disrupts microtubule anchorage rather than transport, alters apical constriction morphodynamics and modulates adherens junction remodelling during amnioserosa cell delamination. The defects we observe are additionally sensitive to ECadherin levels and lead to compromised amnioserosa integrity and adverse dorsal closure outcomes. We suggest that the Dynein-Dynactin complex influences cell morphodynamics in the amnioserosa by enabling the regulation and spatiotemporal coordination of cell adhesion, the mechanistic basis for which remains to be discovered.