During development two-dimensional epithelial sheets fold into three-dimensional structures. In many cases, such as the vertebrate neural tube and Drosophila gastrulation, epithelial cells constrict their apical surfaces, which coupled with a lack of constriction, or even expansion, of the basal domain is thought to cause epithelial folding. In Drosophila gastrulation, the ventral epithelium, or presumptive mesoderm, folds in response to the expression of two embryonic transcription factors, Twist and Snail. Here, we use quantitative microscopy to measure the pattern of gene activation, signaling, myosin activation, and cell shape in the ventral mesoderm. We used in situ hybridization to measure the distribution of Twist mRNA before and during tissue invagination. Next, we measured downstream signaling components, including T48 and DRhoGEF2, using fluorescent fusion proteins under the control of the endogenous promoters. In addition, we have measured the kinetics of non-muscle myosin II accumulation per cell along the dorsal-ventral axis within the ventral region. We have identified multiple mutations in the pathway downstream of Twist that lead to phenotypically similar defects in furrow morphology, some of which prevent invagination. We are testing whether these mutants disrupt the normal spatial pattern of contractility across the ventral mesoderm.