ZFIN ID: ZDB-PUB-010918-6
The slow mo mutation reduces pacemaker current and heart rate in adult zebrafish
Warren, K.S., Baker, K., and Fishman, M.C.
Date: 2001
Source: American journal of physiology. Heart and circulatory physiology   281(4): H1711-H1719 (Journal)
Registered Authors: Fishman, Mark C., Warren, Kerri S.
Keywords: bradycardia; genetic screen; Ih
MeSH Terms:
  • Animals
  • Atrial Function
  • Bradycardia/genetics
  • Bradycardia/physiopathology
  • Cells, Cultured
  • Electrophysiology
  • Heart Conduction System/physiopathology*
  • Heart Rate*
  • Mutation/physiology*
  • Myocardium/cytology
  • Sodium Channels/physiology
  • Ventricular Function
  • Zebrafish/genetics*
PubMed: 11557562
Genetic studies in zebrafish have focused on embryonic mutations, but many physiological mechanisms continue to mature after embryogenesis. We report here that zebrafish homozygous for the mutation slow mo can be raised to adulthood. In the embryo, the slow mo gene is needed to regulate heart rate, and its mutation causes a reduction in pacemaker current (I(h)) and slowing of heart rate (bradycardia). The homozygous adult slow mo fish continues to manifest bradycardia, without other evident ill effects. Patch-clamp analysis of isolated adult cardiomyocytes reveals that I(h) has chamber-specific properties such that the atrial current density of I(h) is far greater than the ventricular current density of I(h). I(h) is markedly diminished in cardiomyocytes from both chambers of slow mo mutant fish. Thus I(h) continues to be a critical determinant of pacemaker rate even after adult neural and humoral influences have developed. It is clear that zebrafish may be used for genetic dissection of selected physiological mechanisms in the adult.