Suppression of Tryptophan 2,3-Dioxygenase Produces a Slow Heartbeat Phenotype in Drosophila melanogaster.

The primary pathway utilizing tryptophan leads initially to kynurenine before branching. Products include nicotinamide adenine dinucleotide and important pigments in the eye. Products in this pathway have been linked to a number of pathologies. The gene encoding the first step in this pathway, tryptophan 2,3-dioxegenase, is encoded by the gene vermilion, initially discovered in Drosophila. In the fly, v is an important eye color marker, but is found to have multiple pleiotropic effects. We have uncovered significant effects of this mutation on the fly heart. The heart beats more slowly and more rhythmically in both males and females and in strains which we have outcrossed. In addition, the fly heart normally beats irregularly with multiple brief stoppages, and the time structure of these stoppages, as investigated by looking at interbeat intervals, is changed in flies bearing this mutation. Fewer flies bearing the v(1) mutation show long hiatuses in beat compared to wild type, however, in some strains of the mutant animals that do, the number of stoppages in much greater and the mean duration is longer.