Embryos lacking maternal ptc function (derived from females carrying ptc^ptcII germline clones and fertilised with a wild-type sperm) develop into fertile adults. Somatic gonadal precursor cells form normally in these embryos. The number of pole cells and migration of the pole cells into the interior of the embryo during gastrulation appears normal in these embryos. Defects become evident around stage 10-11; many of the germ cells associate prematurely, forming clumps of varying sizes, while others scatter to different sites through the mesoderm in the posterior half of the embryo. The clumps generally persist, and are seen associated with the endoderm in the middle of the embryos at stage 13 (by which time the germ cells should have already migrated laterally through the mesoderm). The primitive gonad usually has fewer germ cells than normal. An unusually large number of germ cells are seen in stage 9-10 embryos, suggesting that they are defective in maintaining the cell cycle arrest at the G2/M transition. The increase in cell number is only evident after the germ cells have traversed the midgut. Embryos lacking both maternal and zygotic ptc function (derived from females carrying ptc^ptcII germline clones and fertilised with a ptc^ptcII sperm) show severe segmentation defects, having a naked cuticle.