Gβ13f and Gγ1 act downstream of tre1 in transepithelial migration. (A and B) Phenotype of maternal Gβ13f and Gγ1 mutants. Loss of maternal Gβ13f and Gγ1 results in gastrulation defects and prevents normal germ cell migration. (C) A strategy to rescue the gastrulation phenotype by overexpression of G proteins in the somatic tissue. In the wild type, the product of the G protein X (green) is provided maternally in germ cells and the soma, and is lost from both tissues in maternal G protein X mutants. G protein X product is restored only in the soma by using a soma-specific Gal4 transgene, nullo-GAL4 (yellow), which binds to UAS to turn on transcription in the soma but not in germ cells. (D–O) Phenotype of germ cell migration in the wild type (D–F) and maternal Gβ13f (G–I) and Gγ1 (J–L) mutants with somatic rescue. In these mutants, germ cells (brown, anti-Vasa antibody) display a transepithelial migration defect similar to tre1 mutants (M–O). Embryos are oriented anterior to the left, lateral views except for stage 13 embryos, which are oriented dorsally. Bar, 50 μm.