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Figure 3
The transcription factors Fos and Foxo are required for UV-induced apoptosis in Drosophila. (A) Constitutive activation of JNKK (Hep) in the fly retina results in a 'rough' eye phenotype (expressed in photoreceptors and cone cells under the control of sep-Gal4). This eye phenotype (referred to as SH throughout) requires the downstream kinase, JNK (not shown). (B–D) The forkhead transcription factor FOXO genetically interacts with the JNK pathway. Heterozygosity for the loss-of-function allele dfoxo21 suppresses the JNK gain-of-function phenotype (B), whereas co-overexpression of Foxo greatly enhances the eye phenotype (C). Overexpression of Foxo alone with sep-Gal4 does not impact eye morphology (D). (E–G) Similarly, decreasing Fos function by introducing the loss-of-function mutation kay2 (E), or by co-overexpressing dsRNA against Fos (F), rescues the sep>Hepact phenotype. Reducing both dfoxo and kay gene dose (G) results in an almost full recovery of normal eye morphology. (H, I, N) Homozygosity for the dfoxo loss-of-function allele dfoxo25 reduces UV-induced apoptosis. Treatment and quantification were performed as described in Figure 1. (J–N) Increased Fos expression (M, N) enhances, and loss of fos function (J, L, N) reduces UV-induced apoptosis in the eye, as compared to wild-type controls (K, N).
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