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 fully understood. Non-muscle myosin II (Myosin II) is an important force generator in many cell and tissue types that acts through its contraction on actin network. In this study, we identify an actomyosin activity-dependent mechanism involving Rab11-mediated trafficking in regulating apical constriction in the Drosophila embryo. During Drosophila mesoderm invagination, apical actin and Myosin II (actomyosin) contractility induces accumulation of Rab11-marked vesicle-like structures (“Rab11 vesicles”) near the apical membrane. These Rab11 vesicles are not derived from apical endocytosis. Instead, apical accumulation of Rab11 vesicles is associated with constant vesicle transport along cell apical-basal axis, which is mediated by microtubule motor dynein. Interestingly, actomyosin contractility promotes apical targeting of Rab11 vesicle by inhibiting the reverse transport, the resulting directional bias towards apical side therefore contributes to the apical accumulation of Rab11 vesicles. 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 therefore promotes the stepwise, ratchet-like cell area reduction and overall apical constriction. This function of Rab11 is separate from its earlier role in promoting apical Myosin II accumulation. These findings suggest a feedback mechanism between actomyosin-mediated apical constriction and Rab11-mediated intracellular trafficking that regulates the force generation machinery during tissue folding.