Abstract - Tissue morphogenesis requires force-generating mechanisms to drive the organization of cells into complex three-dimensional structures^1-3. Although such mechanisms have been characterized across the metazoan lineage, we know little about how force transmission across a tissue is regulated. Here, we provide evidence that integrin-mediated Cell-ECM adhesion is required for the regulation and transmission of forces in tissues. Specifically we show that during Dorsal Closure (DC), an integrin-dependent morphogenetic process⁴, failure to regulate the level of Cell-ECM adhesion results in abnormal levels of tension in the amnioserosa (AS), an extra-embryonic epithelium that is essential for DC⁵. Integrin-containing adhesive structures were identified on the basal surface of the AS that share many features with focal adhesions. Using mutations that either increase or decrease integrin-based Cell-ECM adhesion, we show that DC is defective in both cases, and that the level of adhesion is inversely correlated with the mobility of cells in the AS. Mathematical modeling, quantitative image analysis, and in vivo laser ablation experiments reveal a relationship between cell mobility and the magnitude and distribution of tension in the AS. Overall, our data suggests that integrins regulate cell mobility, which is essential in allowing tension to be transmitted and distributed within developing tissues. We propose that modulating Cell-ECM adhesion could provide rheostatic control over force within developing tissues to promote specific outcomes.