ZFIN ID: ZDB-PUB-121030-7
Analysis of post-embryonic heart development and maturation in the zebrafish, Danio rerio
Singleman, C., and Holtzman, N.G.
Date: 2012
Source: Developmental dynamics : an official publication of the American Association of Anatomists   241(12): 1993-2004 (Journal)
Registered Authors: Holtzman, Nathalia Glickman
Keywords: heart development, cardiac maturation, zebrafish, danio rerio, ventricle, atrium, trabeculation, bulbous ateriosus, congenital heart disease, myh6, weak atrium
MeSH Terms:
  • Animals
  • Heart Atria/embryology
  • Heart Defects, Congenital/embryology
  • Heart Defects, Congenital/etiology
  • Heart Defects, Congenital/genetics
  • Heart Ventricles/cytology
  • Heart Ventricles/embryology*
  • Mutation
  • Myocardium/cytology
  • Myocardium/metabolism*
  • Myosin Heavy Chains/genetics
  • Myosin Heavy Chains/metabolism
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
PubMed: 23074141 Full text @ Dev. Dyn.


Cardiac maturation is vital for animal survival and must occur throughout the animal's life. Zebrafish are increasingly used to model cardiac disease; however, little is known about how the cardiovascular system matures. We conducted a systematic analysis of cardiac maturation from larvae though to adulthood and assessed cardiac features influenced by genetic and environmental factors.


We identified a novel step in cardiac maturation, termed cardiac rotation, where the larval heart rotates into its final orientation within the thoracic cavity with the atrium placed behind the ventricle. This rotation is followed by linear ventricle growth and an increase in the angle between bulbous arteriosus and the ventricle. The ventricle transitions from a rectangle, to a triangle and ultimately a circle that is significantly enveloped by the atrium. In addition, trabeculae are similarly patterned in the zebrafish and humans with both muscular fingerlike projections and muscle bands that span the cardiac chamber. Interestingly, partial loss of atrial contraction in myosin heavy chain 6 (myh6/weahu423/+) mutants result in the adult maintaining a larval cardiac form.


These findings serve as a foundation for the study of defects in cardiovascular development from both genetic and environmental factors.