[Myc and cell competition in Drosophila].

Cell differentiation and organ shaping proceed not only upon instructive but also upon competitive cell-cell interactions. In the proliferating epithelium forming the larval Drosophila wing disc, cell competition contributes to the fidelity of the organogenesis. Several recent studies show how d-myc, encoding a bHLH/LZ transcription factor homologous to vertebrate Myc proteins, controls cell competition during wing development. In this model, any experiment leading to the confrontation of two populations differing by their levels of d-Myc expression, even in a two-fold ratio, gives rise to a competition characterized both by an overgrowth of the population having the highest level and an apoptotic elimination of the neighbouring << weakly >> expressing cells. As a consequence of the mutually compensating nature of these two processes, the final size of the wing remains unchanged. Importantly, lowering or elevating d-Myc expression to the same extent in all cells of the disc does not trigger competition. This indicates that competition is linked to a spatial heterogeneity in, and not to the absolute level of, d-Myc expression. Both vertebrate and Drosophila Myc proteins stimulate ribosome biogenesis, and genetic evidence in Drosophila suggests that this property underlies the strong competitive advantage imparted by its relatively high expression. Accordingly, it is proposed, although not proved, that the more the wing cells express d-Myc and amplify their protein synthesis apparatus, the more they bind, internalize, and transduce the vital and limiting growth factor Dpp, which in turn is presumed to increase d-Myc protein level. These findings suggest that wing organogenesis is a self-corrected process whereby d-Myc induction in overgrowing cells ensures the compensatory elimination of their neighbours. Moreover, they have important implications for the oncogenic role of vertebrate Myc proteins and possibly of related transcription factors.