MOLECULAR-BASIS OF INTRACISTRONIC COMPLEMENTATION IN THE PASSOVER LOCUS OF DROSOPHILA

The only demonstrated mechanism for intracistronic genetic complementa tion requires physical interaction of protein subunits to create a fun ctional molecule. We demonstrate another and perhaps quite general mec hanism utilizing proteins with unique and shared domains. The Drosophi la neural mutant Passover (Pas) disrupts specific synaptic connections . Alleles of a lethal complementation group exhibit a complex pattern of complementation with Pas alleles. Whereas ail heterozygotes between these lethal alleles and Pas are viable, only some alleles complement the neural defect of Pas. Lethal and neural functions are separately encoded by two proteins that have distinct N-terminal domains and a co mmon C-terminal portion. Neural-specific and lethal-specific mutations map to unique exons, while neural-lethal mutations map to shared exon s. Combinations of lethal and neural alleles result in production of b oth proteins and demonstrate intracistronic complementation.