View Program - 63rd Annual Drosophila Research Conference

Congenital heart defects are the most prevalent birth defect presented in the human population. A number of these cases have been ruled as sporadic, or resulting from different interactions of many independent genetic loci and alleles. Gene combinations and chromosomal changes are known to play a crucial role in the development of congenital heart defects, but the precise genetic and environmental factors involved in this process remain poorly understood. In Drosophila, the process of heart specification and patterning is controlled by a number of transcription factors that work together with the nuclear co-factor, Akirin, to mediate cardiac gene expression. Preliminary work in the Nowak Laboratory found that Akirin likely regulates gene expression by working together with the Nucleosome Remodeling and Deacetylase (NuRD) complex. Embryos bearing mutations in different NuRD subunits produce hearts, but they are often severely misshapen, poorly patterned, and have reduced numbers of cardiomyoblasts. Moreover, quantitative live imaging of cardiac contractions in pre-hatching embryos indicates that these hearts display impaired cardiac function. Together, these data suggest that Akirin/NuRD interactions may be key regulators of proper heart function.

The role of Akirin/NuRD interactions during heart development