Summary
During tissue morphogenesis, cell shape changes resulting from cell-generated forces often require active regulation of intracellular trafficking. How mechanical stimuli influence intracellular trafficking and how such regulation impacts tissue mechanics are not understood. We identify a mechanosensitive mechanism involving Rab11 recycling endosomes in regulating apical constriction in the Drosophila embryo. During Drosophila mesoderm invagination, apical actin and myosin II (actomyosin) contractility induces accumulation of Rab11-marked vesicles near the apical membrane by promoting a directional bias in vesicle transport, which is mediated by the microtubule motor dynein. At the apical domain, Rab11 vesicles are targeted to the adherens junctions (AJs). The apical accumulation of Rab11 vesicles is essential to prevent fragmented apical AJs, breaks in the supracellular actomyosin network and a reduction in the apical constriction rate, which is separate from the function of Rab11 in promoting apical myosin II activation. These findings provide evidence for a mechanosensitive feedback mechanism between actomyosin-mediated apical constriction and Rab11-mediated intracellular trafficking that regulates the force generation machinery during tissue folding.
Competing Interest Statement
The authors have declared no competing interest.