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Fig. 7. Loss of L gene function results in activation of the JNK signaling pathway. (A) In L²/+ eye disc, puc-lacZ, a reporter for JNK signaling pathway activation, is ectopically induced on the ventral eye margin. (B,B') In LOF clones of L, ectopic induction of puc-lacZ was observed in only the ventral eye margin (arrows). In the dorsal eye clones, puc-lacZ was not induced (arrowheads). (C-D') Blocking JNK signaling by overexpression of puc (Martin-Blanco et al., 1998) in the eye does not affect eye size (C), whereas, in L²/+-mutant eyes, it rescues the ventral eye loss in the eye imaginal disc (D) and adult eye (D'). (E) Overexpression of a dominant-negative form of Bsk (Bsk^DN) alone in the eye served as control. (F,G) Reducing levels of JNK signaling by overexpressing Bsk^DN (F) or by using a heterozygous background of a null mutant of hep (hep/+; L²/+; G) rescues the L-mutant eye phenotype. (H-I') Increasing levels of JNK signaling by overexpressing the activated form of Bsk (Bsk^Act) in wild-type eye (H) results in small eye but, in L²/+-mutant eye (I,I'), it causes severe enhancement of the loss-of-ventral-eye phenotype. (J-K') Overexpression of the activated form of Drosophila Jun in the wild-type (J) does not affect the eye. However, overexpression of Drosophila Jun strongly enhances the L²/+-mutant phenotype (K,K') in the eye. Dashed lines mark the lost boundary of the eye field. AN, Antenna.

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