Fig. 7. ß-Spectrin regulates -Spectrin stability. Top three panels show eye imaginal discs with homozygous-mutant cell clones lacking ß-Spectrin (red) or -Spectrin (white), as indicated. Single confocal planes are shown. Clones were induced by expressing flp under the eyeless promoter and are marked by either the lack of GFP expression (green) or the loss of Spectrin expression. (A) In cell clones that are homozygous-mutant for the strong hypomorphic allele ß-spectrin^G113, significantly reduced levels of ß-spectrin can be detected that appear to localize normally at the cell cortex. Concomitant to the reduction of ß-Spectrin expression we noticed a reduction in the level of -Spectrin. (B) Similar results were obtained for cells homozygous for the ß-spectrin^E292 mutation. (C) Clones homozygous for the strong -spectrin allele D4-65 lack -Spectrin protein expression but ß-Spectrin expression is not affected. Almost the entire eye is mutant for -spectrin, except for a small area (arrow). (D) Wing imaginal disc expressing the UAS-ß-spectrin construct under the control of the patched::Gal4 driver. Elevated levels of ß-Spectrin result in a concomitant up-regulation in the level of -Spectrin.