Fig. 3. Ci is dispensable for the patterning and progression of eye differentiation. (A) Ci155 in magenta; atonal in green. Initiation and progression of Atonal expression occurs normally in cells deleted for the ci gene. (B) Clones of cells lacking both eye pigmentation and Ci function contribute to normal adult eye structures (arrows). (C) Normal ommatidia are seen in sections through ci-null mutant clones marked by unpigmented pigment cells. A basal plane of section is shown so that normal R8 differentiation is apparent (arrows). The equator runs through the ci-mutant region. (D) Morphogenetic furrow progression is retarded through smo-mutant cells. The product of the Atonal target gene sens reveals both Atonal activity and subsequent differentiation of R8 cells (green). Cells mutant for smo lack the clone marker (magenta) and are also mutant for engrailed (en), a gene that is not required during eye development (Strutt and Mlodzik, 1996), see panel E. (E) Senseless expression and progression (green) occur completely normally in smo ci-mutant cells (also mutant for en). The clone is similar in size to the smo clone in panel E, induced simultaneously in a sibling larva (see Materials and methods for details). (F) Fng:Gal4 drives UAS-lacZ reporter gene expression in the ventral eye disc anterior to the morphogenetic furrow. Fng:Gal4 also drives expression more weakly in the posterior dorsal eye disc, away from the equator, expanding to reach the equator and morphogenetic furrow in the late third instar (Cho and Choi, 1998; Dominguez and de Celis, 1998; Papayannopoulos et al., 1998) (M. Mlodzik, personal communication). (G) Ventral Ci75 expression retards furrow progression (arrowhead shows position of furrow dorsally, arrow indicates ventral delay).