The formation of the ventral furrow during Drosophila gastrulation is driven by coordinated apical constriction. Cell-cell adhesion is thought to regulate apical constriction, but the mechanisms are poorly understood. DE-cadherin, an epithelial classic cadherin, has in its membrane-proximal extracellular region a suite of domains absent from vertebrate/urochordate classic cadherins. We constructed DEDeltaP, a DE-cadherin derivative that lacks the membrane-proximal half of the extracellular region but retains the entire cytoplasmic domain and still exhibits strong cell-cell binding ability. The extracellular region of DEDeltaP consists of only cadherin repeats, mimicking vertebrate/urochordate classic cadherins. In animals lacking DE-cadherin, DEDeltaP organized adherens junction assembly and functioned fully in many cadherin-dependent processes, including oogenesis. Embryos in which DE-cadherin was entirely replaced by DEDeltaP established the blastoderm epithelium but failed to form a ventral furrow. Apical constrictions were initiated relatively normally but subsequently decelerated. These were then followed by catastrophic disruption of the junctional network. Our results suggest that although the membrane-proximal half of the DE-cadherin extracellular region is dispensable for many developmental events, it is essential for efficient and robust apical constriction during ventral furrow formation.