Figure 7.

Aberrant JNK signaling in cul-4 loss-of-function background triggers cell death. (a) A functional readout of JNK signaling pathway, puc-lacZ (blue) is expressed in differentiated photoreceptor neurons (marked by Elav, red) in the wild-type eye discs.⁶⁰ (b and b') Loss-of-function of cul-4 causes ectopic induction of puc-lacZ reporter in the eye imaginal disc. (c) Activation of JNK signaling was detected by analyzing phospho-Jun (p-JNK) levels in western blots. Twofold increase in the levels of JNK signaling pathway was detected in cul-4 loss-of-function backgrounds in comparison to the wild-type eye imaginal disc. (d–i) Blocking JNK signaling by misexpression of (e, e' and f) puc (cul-4^−/−; ey>puc) or (h, h' and i) dominant negative bsk^DN(cul-4^−/−; ey>bsk^DN) in loss-of-function clones of cul-4 significantly restores their reduced eye phenotype as seen in the (e, e', h and h') eye imaginal disc and the (f and i) adult flies. Misexpression of (d) puc (ey>puc) or (g) bsk dominant negative (ey>bsk^DN) does not affect the eye size. (j–l) Misexpression of activated form of (j) jun (ey>jun^aspv7) in the developing eye results in reduced eye size, whereas (k, k' and l) misexpression of activated jun (cul-4^−/−; ey>jun^aspv7) results in further enhancement of cul-4 loss-of-function phenotype of reduced eye