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The EMBO Journal (2007) 26, 380–390, doi:10.1038/sj.emboj.7601484 Published online 21 December 2006 Figure 5 Foxo and Fos regulate the decision between cell death and survival in response to UV irradiation Xi Luo, Oscar Puig, Joogyung Hyun, Dirk Bohmann and Heinrich Jasper

Figure 5 EGFR and Insulin signaling suppress JNK-mediated apoptosis. Decreased level of EGFR activity by mutations in either EGFR (B) or ras (C) and reduced insulin signaling owing to loss of chico (D) substantially enhances the apoptotic phenotype induced by overexpression of Hepact (A). Similarly, the eye phenotype induced by Foxo overexpression (E) is enhanced by reduced EGFR (F) or ras gene dose (G). Conversely, blocking Foxo activity by co-overexpressing Akt or active PI3K blocks the Foxo gain-of-function phenotype (H, I). (J–O) UV-induced apoptosis is reduced by EGF/insulin-mediated survival signaling. Reduced activity of ras (K, O) or chico (M, O) results in strongly increased UV-induced defects in the eye. Conversely, loss of aos, a negative regulator of EGFR, or increased expression of InR, decreases UV-induced apoptotic defects (L, N, O). Genotypes are as follows: A, w; sep-Gal4, UAS-Hepact/+; B, w; sep-Gal4, UAS-Hepact/egfrf2; C, w; sep-Gal4, UAS-Hepact/+; rase1B/+; D, w; sep-Gal4, UAS-Hepact/chico1; E: w; GMR-Gal4, UAS-Foxo/+; F, w; GMR-Gal4, UAS-Foxo/egfrf2; G, w; GMR-Gal4, UAS-Foxo/+; rase1B/+; H, w; GMR-Gal4, UAS-Foxo/UAS-Akt; I, w; GMR-Gal4, UAS-Foxo/UAS-PI3Kact; J, OreR. K: rase1B/TM3; L, aos7/TM3; M, chico1/chico1; N, w1118; sep-Gal4/UAS-InR.

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