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The GATA transcription factor encoded bypannier(pnr) is a critical regulator of heart progenitor formation inDrosophila. Mutations inGATA4, the mammalian homolog ofpnr, have also been implicated in causing human cardiac disease in a haploinsufficient manner. Mouse models ofGata4loss-of-function and gain-of-function studies underscored the importance ofGata4in regulating cardiac progenitor cells specification and differentiation. However, it is not known whetherpnr/Gata4is directly involved in establishing and maintaining adult heart physiology because of the lethality associated with defective heart function and redundancy among various GATA factors in vertebrates. Here, we took advantage of theDrosophilaheart model to examine the function ofpnrin adult heart physiology. We found thatpnrheterozygous mutants result in defective cardiac performance in response to electrical pacing of the heart as well as in elevated arrhythmias. Adult-specific disruption ofpnrfunction using a dominant-negative formpnrEnR revealed a cardiac autonomous requirement ofpnrin regulating heart physiology. Moreover, we identifiedTbx20/neuromancer(nmr) as a potential downstream mediator ofpnrin regulating cardiac performance and rhythm regularity, based on the observation that overexpression ofnmrgenes, but not oftinman, partially rescues the adult defects inpnrmutants. We conclude thatpnris not only essential for early cardiac progenitor formation, along withtinmanand T-box factors, but also plays an important role in establishing and/or maintaining proper heart function, which is partially through another key regulatorTbx20/nmr.

Partial loss of GATA factor Pannier impairs adult heart function in Drosophila