A congenital heart defect in Drosophila caused by an action-potential mutation

J Neurogenet. 1995 Dec;10(3):153-68. doi: 10.3109/01677069509083461.

Abstract

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

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Action Potentials / genetics
  • Animals
  • Arrhythmias, Cardiac / genetics*
  • Arrhythmias, Cardiac / physiopathology
  • Drosophila Proteins
  • Drosophila melanogaster / genetics*
  • Drosophila melanogaster / growth & development
  • Epistasis, Genetic
  • Genes, Insect*
  • Heart Conduction System / physiopathology*
  • Heart Rate / genetics
  • Larva
  • Myocardial Contraction / genetics
  • Nuclear Proteins / genetics
  • Nuclear Proteins / physiology
  • Period Circadian Proteins
  • Phenotype
  • Sodium Channels / genetics
  • Sodium Channels / physiology
  • Temperature

Substances

  • Drosophila Proteins
  • Nuclear Proteins
  • PER protein, Drosophila
  • Period Circadian Proteins
  • Sodium Channels
  • para protein, Drosophila