Drosophila melanogaster as a model system for genetics of postnatal cardiac function

Abstract

The fruit fly, Drosophila melanogaster, is an excellent model system that has a vast set of molecular tools and mutants to dissect the genetic pathways that are responsible for the normal and abnormal cardiac function. While the majority of studies have focused on heart development in the Drosophila embryo, attention has recently focused on the structure and function of the adult fly heart as a model of human heart failure. Here we review strategies to identify novel genes and pathways that cause or modify dilated cardiomyopathy in adult Drosophila.

Figure 1

OCT images of cardiac chamber in adult w1118 Drosophila. (A) Schematic representation of the cardiac chamber (red box) of an adult Drosophila based on Miller [45]. (B) Longitudinal and transverse B-mode OCT images of the cardiac chamber in adult Drosophila during diastole and systole. (C) Representative m-mode OCT image demonstrating the cardiac cycle with diastole and systole denoted by the red arrows.

Figure 2

Screening cardiac function in adult Drosophila by OCT identifies mutants with dilated cardiomyopathy. End-diastolic dimension (EDD), end-systolic fraction (ESD), and fractional shortening defined as (EDD-ESD)/EDD are shown for a series of mutants with deficiencies along the 3L chromosome. The red lines represent measurements that are two standard error units outside the mean for w1118 flies cardiac measurements that were used as controls. A series of mutants with dilated cardiomyopathy or impaired systolic function with preserved diastolic dimensions can be readily identified.