Genetic interactions between Protein Kinase D and Lobe mutants during eye development of Drosophila melanogaster

Abstract

AbstractBackgroundInDrosophila,the development of the fly eye involves the activity of several, interconnected pathways that first define the presumptive eye field within the eye anlagen, followed by establishment of the dorso-ventral boundary, and the regulation of growth and apoptosis. InLobe (L)mutant flies, parts of the eye or even the complete eye are absent because the eye field has not been properly defined. Manifold genetic interactions indicate thatLinfluences the activity of several signalling pathways, resulting in a conversion of eye tissue into epidermis, and in the induction of apoptosis. As information on the molecular nature of theLmutation is lacking, the underlying molecular mechanisms are still an enigma.ResultsWe have identified Protein Kinase D (PKD) as a strong modifier of theLmutant phenotype. PKD belongs to the PKC/CAMK class of Ser/Thr kinases that have been involved in diverse cellular processes including stress resistance and growth. Despite the many roles of PKD,Drosophila PKDnull mutants are without apparent phenotype apart from sensitivity to oxidative stress. Here we report an involvement ofPKDin eye development in the sensitized genetic background ofLobe. Absence ofPKDstrongly enhanced the dominant eye defects of heterozygousL2flies, and decreased their viability. Moreover, eye-specific overexpression of an activated isoform of PKD considerably ameliorated the dominantL2phenotype. This genetic interaction was not allele specific but similarly seen with three additional, weakerLalleles (L1, L5, LG), demonstrating its specificity.ConclusionsWe propose that PKD-mediated phosphorylation is involved in underlying processes causing theLphenotype, i.e. in the regulation of growth, the epidermal transformation of eye tissue and apoptosis, respectively.