Cardiac remodeling in Drosophila arises from changes in actin gene expression and from a contribution of lymph gland-like cells to the heart musculature.

Understanding the basis of normal heart remodeling can provide insight into the plasticity of the cardiac state, and into the potential for treating diseased tissue. In Drosophila, the adult heart arises during metamorphosis from a series of events, that include the remodeling of an existing cardiac tube, the elaboration of new inflow tracts, and the addition of a layer of longitudinal muscle fibers. We have identified genes active in all these three processes, and studied their expression in order to characterize in greater detail normal cardiac remodeling.

Cardiac expression of the Drosophila Sulphonylurea receptor gene is regulated by an intron enhancer dependent upon the NK homeodomain factor Tinman.

Cardiac development proceeds via the activation of a complex network of regulatory factors which both directly and indirectly impact downstream cardiac structural genes. In Drosophila, the NK homeodomain transcription factor Tinman is critical to cardiac specification and development via the activation of a number of key regulatory genes which mediate heart development. In this manuscript, we demonstrate that Tinman also functions in Drosophila to directly activate transcription of the ATP binding cassette gene Sulphonylurea receptor (Sur).