Fig. 2. Egg chambers that contain both follicle cell and germline clones mutant for papss produce dorsalized embryos. (A,C,E,G) Whole-mount stainings of syncytial blastoderm embryos with anti-Twist antibody. (B,D,F,H) Cuticle preparations of developed embryos. (A,B) Embryos from wild-type mothers. (C,D) Embryos from e22c-GAL4, UAS-FLP/+; FRT^82B hGFP/FRT^82B sll^7E18mother carrying homozygous sll mutant follicle cell clones. Anterior Twist expression is disrupted (C) and the cuticle is dorsalized (D). (E,F) Embryos from hsFLP1/+; P[ovo^D1] FRT^79D/papss² FRT^79D mothers mated to wild-type males. Loss of papss from the germline alone does not affect Twist expression (E) or DV pattern formation of the embryo (F). Paternally-rescued embryos exhibit weak segmentation defects (F), similar to paternally-rescued embryos derived from sgl mutant germline clones (Binari et al., 1997; Perrimon et al., 1996). (G,H) Embryos from hsFLP1/+; e22c-GAL4, UAS-FLP/+; P[ovo^D1] FRT^79D/papss² FRT^79D mothers mated to wild-type males. Loss of papss function in both the germline and the follicular epithelium disrupts Twist expression (G) and results in embryos that lack ventral and lateral pattern elements (H).