Mutation in Rab11 results in abnormal organization of ommatidial cells and activation of JNK signaling in the Drosophila eye

Rab11mo, a P insertion line of Rab11 showed degenerated ommatidia and excess cell death in larval/pupal eyes. Here, we demonstrate that Rab11 is essential for normal organization of ommatidial cells and their survival in Drosophila, and a mutation in this gene results in cytoskeleton disruption and activation of JNK signaling in the eye. The spatial organization of various cell types in compound eye, viz., cone, photoreceptor, pigment and bristle cells, were disrupted in Rab11 mutants as revealed by immunostaining of F-actin and adherens and septate junction proteins. Genetic interaction studies indicated that mutation in Rab11 upregulates Drosophila apoptotic genes, rpr, hid and grim. In order to study the pathway that causes excessive cell death in Rab11 mutants, the JNK pathway was chosen and genetic interaction analyses were carried out between Rab11 and candidates of the JNK signaling pathway. A downregulation of JNK signaling rescued the phenotype in Rab11 mutant eyes significantly while overexpression of JNK in the eyes using UAS-eiger, UAS-dtak1 or EP(2)0578, resulted in enhancement of the eye phenotype indicating a link between Rab11 and the JNK signaling pathway.