The transcription factor, Mycn, is known to play an essential function in heart development, as demonstrated by cardiac-specific deletion of the Mycn gene. A related protein, Myc, was also widely believed to function in cardiogenesis based on data from global knockouts or overexpression. However, Myc had not been deleted specifically in the developing heart. Now, Miguel Torres and colleagues generate and analyse conditional Myc mouse mutants to provide compelling evidence that Myc is dispensable for homeostatic growth of the heart. The authors show that, unlike Mycn, cardiac-specific deletion of Myc does not affect heart development. Indeed, they find that Myc is expressed in endothelial cells, but not in developing cardiomyocytes. Interestingly, ectopic mosaic expression of Myc in the heart is able to functionally compensate for loss of Mycn in a cell-autonomous fashion. In addition, Myc rescues global heart development through cell competition, whereby Mycn-deficient cells are replaced with Myc-rescued neighbours. This research confirms a number of previously reported findings about Myc family member roles in the heart and reveals novel insights into how Myc-driven cell competition occurs. Furthermore, the study highlights cell competition as a potential physiological mechanism for eliminating unfit cardiomyocytes during cardiogenesis.
