Fig. 4. shg/E-cadherin mutants have defects in gonad compaction, germ cell ensheathment and germ cell migration. Anterior is leftwards, embryos are stage 15 or later. Vasa labels the germ cells in B-D,F. (A,B) shg^G317 homozygous embryos. (A) SGPs labeled with EYA. Example of a strong gonad compaction defect. shg mutants also display defects in germ cell migration, and the gonad in A lacks germ cells completely (Vasa channel not shown). (B) EYA marks the SGPs. Example of a weak gonad compaction defect. (C) Stage 15 wild-type male. msSGPs (arrow) express EYA and Sox100B, while SGPs express only EYA. msSGPs join the posterior of male gonads. (D) shg^G317 homozygous male embryo. msSGPs have failed to join the gonad, remaining in a tight cluster posterior to the gonad (arrow). (E) shg^G317 homozygous embryo. UAS-mCD8-GFP expressed in the mesoderm (24B-Gal4) labeled with anti-GFP and anti-EYA. The lack of GFP-labeled SGP extensions between the germ cells indicates a failure of germ cell ensheathment. (F) Stacked z-series through an embryo from a cross of shg^G317/CyOftz-lacZ females and w¹¹¹⁸ males that did not inherit the shg^G317 chromosome zygotically. Anti-EYA (not shown) was used to identify the normal position of the one gonad visible in this image (circle). Many lost germ cells are observed, indicating a dominant maternal effect of shg^G317 on germ cell migration. Scale bar in A: 10 µm.