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Fig. 2. Cholesterol-modification of Hh is necessary for Hh-dependent graded cell fate specification in the dorsal epidermis. All panels show dorsal cuticle views of first instar larvae. (A) Wild type. (B) hh^AC. (C) hh^AC, engal4 UAS-hh-Np. (D) hh^AC, engal4 UAS-hh-N-CD2. (E) hh^AC, engal4 UAS-hh-N. (F) ptcgal4 UAS-Shi^DN. (G) disp glc. (H) disp glc, enGal4 UAS-hh-Np and (I) disp glc, enGal4 UAS-hh-N. (A) In the wild-type dorsal epidermis, Hh is secreted from type 1 cells and forms a morphogen gradient that allows the differentiation of cell types 1 to 3 in a concentration-dependent manner (scheme and cuticle). (B) In hh loss of function, only type 4 cells are present. (C) Expression of Hh-Np in En cells allows the rescue of the hh mutant phenotype. (D,E) Hh-N or Hh-N-CD2 expression induces some type 1 cells and a domain of type 2 cuticle, but in the case of Hh-N-CD2 naked cuticle was never formed at the midline (broken line in D). (F) In ptcgal4 UAS-Shi^DN larvae, the domain of type 2 cells is reduced, whereas the domain of type 3 cells is enlarged. (G) In disp glc loss of function, only type 4 cells are present. (H,I) In disp glc embryos, Hh-Np only induced some patches of type 1 cells (arrow in H), whereas Hh-N induced type 1 and some type 2 cells. Bars delimit the width of type 2 cuticle. (J) Histogram showing the width of the cuticle covered by type 2 and 3 cells in the genotypes shown in A,C-F. (K) A theoretical model based on the results shown in J, representing cell fate behaviours as a function of Hh range and activity. Numbers correspond to the type of fate adopted by the dorsal cells related to the distance from Hh-producing cells.

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