spitz, a Drosophila homolog of transforming growth factor-alpha, is required in the founding photoreceptor cells of the compound eye facets.

Cell type specification and differentiation in the developing Drosophila compound eye begins in the morphogenetic furrow. In the furrow, cells are organized into evenly spaced preclusters and there is a synchronized arrest of the cells' mitotic cycle in G1. We report that recessive spitz loss-of-function mutations affect compound eye development. Spitz is homologous to the human transforming growth factor-alpha. In mosaic clones, spitz function is required in the first photoreceptor cells to differentiate for normal ommatidial development. spitz loss-of-function mutations are dominant suppressors of EgfrE gain-of-function mutations of the epidermal growth factor-receptor gene. These data suggest that the spitz product is a precluster promoting factor. spitz transcription increases abruptly in the morphogenetic furrow, the obverse of Egfr expression. We present a model for the expression of, and cellular requirement for, this growth factor homolog.