ZFIN ID: ZDB-PUB-000906-3
The genetic basis of cardiac function: dissection by zebrafish (Danio rerio) screens
Warren, K.S., Wu, J.C., Pinet, F., and Fishman, M.C.
Date: 2000
Source: Philosophical transactions of the Royal Society of London. Series B, Biological sciences   355(1399): 939-944 (Journal)
Registered Authors: Fishman, Mark C., Warren, Kerri S.
Keywords: zebrafish; genetic screen; cardiac development; cardiac function; single-gene mutation; contractility disorder
MeSH Terms: none
PubMed: none
The vertebrate heart differs from chordate ancestors both structurally and functionally. Genetic units of form, termed 'modules', are identifiable by mutation, both in zebrafish and mouse, and correspond to features recently acquired in evolution, such as the ventricular chamber or endothelial lining of the vessels and heart. Zebrafish (Danio rerio) genetic screens have provided a reasonably inclusive set of such genes. Normal cardiac function may also be disrupted by single-gene mutations in zebrafish. Individual mutations may perturb contractility or rhythm generation. The zebrafish mutations which principally disturb cardiac contractility fall into two broad phenotypic categories, 'dilated' and 'hypertrophic'. Interestingly, these correspond to the two primary types of heart failure in humans. These disorders of early cardiac function provide candidate genes to be examined in complex human heart diseases, including arrhythmias and heart failure.