A Congenital Heart Defect in Drosophila Caused by an Action-Potential Mutation

Abstract

The mutation no action potential^{temperature itive} (nap^ts) induces arrhythmia in the heartbeat of Drosophila melanogaster larvae at temperatures above 20°C; heartbeat becomes normally rhythmic again after a shift back to 20°C. For this phenotype, nap^ts is almost completely recessive to the wild type. nap^ts also reduces the temperature-sensitivity of heart rate over a wide range of temperatures, for this phenotype, nap^ts, is dominant over the wild type, nap^ts causes reversible paralysis in adults by epistatic effects on the expression of paralytic, a gene encoding a voltage-dependent sodium channel. However, the para mutation, which induces paralysis in adults at 29°C, has no effect on larval heartbeat at temperatures between 20° and 37.5°C. The period gene, contra earlier reports, has no effect on heartbeat.

Key Words:

• Cardiac arrhythmia
• heartbeat
• spectral analysis no action potential mutant
• period mutant