A Genetic Screen for Synaptic Transmission Mutants Mapping to the Right Arm of Chromosome 3 in Drosophila

Abstract

Neuronal function depends upon the proper formation of synaptic connections and rapid communication at these sites, primarily through the regulated exocytosis of chemical neurotransmitters. Recent biochemical and genomic studies have identified a large number of candidate molecules that may function in these processes. To complement these studies, we are pursuing a genetic approach to identify genes affecting synaptic transmission in the Drosophila visual system. Our screening approach involves a recently described genetic method allowing efficient production of mosaic flies whose eyes are entirely homozygous for a mutagenized chromosome arm. From a screen of 42,500 mutagenized flies, 32 mutations on chromosome 3R that confer synaptic transmission defects in the visual system were recovered. These mutations represent 14 complementation groups, of which at least 9 also appear to perform functional roles outside of the eye. Three of these complementation groups disrupt photoreceptor axonal projection, whereas the remaining complementation groups confer presynaptic defects in synaptic transmission without detectably altering photoreceptor structure. Mapping and complementation testing with candidate mutations revealed new alleles of the neuronal fate determinant svp and the synaptic vesicle trafficking component lap among the collection of mutants recovered in this screen. Given the tools available for investigation of synaptic function in Drosophila, these mutants represent a valuable resource for future analysis of synapse development and function.

Mitochondrial Miro GTPases coordinate mitochondrial and peroxisomal dynamics

“…The critical role of Miro proteins and the associated motor adaptor trafficking kinesin-binding proteins (TRAKs) for mitochondrial transport was first recognized in Drosophila neurons. Independent genetic screens identifying genes necessary for synaptic function discovered mutations in dMiro and the single Drosophila TRAK ortholog Milton [33,77,78]. Loss of either dMiro or Milton caused premature lethality, impaired synaptic transmission, and disrupted the mitochondrial distribution in neurons [33,78].…”