Double mutants of dpp^H48 with sog^YL26 or sog¹ have phenotypes identical to that of the dpp mutant alone.

Embryos hemizygous for sog¹ have the following defects: the initial stage of posterior midgut formation is delayed by about 6 minutes. Germband extension stops about 25-30 minutes after the onset of gastrulation, the dorsal cells form abnormal deep folds and there is a delay in the closing of the anterior and posterior midguts from the surface. The posterior midgut subsequently buckles under the dorsal cells and the folds on the dorsal side of the embryo are released. At the end of gastrulation the amnioserosa forms a thick double sheet folded back over the extended germband on the dorsal side of the embryo. At later stages a small patch of flattened amnioserosa-like cells is seen on the dorsal side of the embryo. The mandibular bud is not seen and severe head defects are seen in the cuticle at the end of embryogenesis.

embryonic lethal weak ventralized phenotype. Invagination and subsequent closing of the posterior midgut and anterior midgut delayed; germ-band extension incomplete; dorsal-most cells fail to assume normal amnioserosal fate; they are abnormally thick and fall into deep dorsal folds at the time of germ-band extension. Mosaic studies indicate that sog expression required only ventrally for normal development. No discernible maternal effect.