Abstract
Cell fate determination in the Drosophila eye is mediated by inductive events between neighboring cells in the eye imaginal disc. These inductive signals lead to differential gene expression necessary for the elaboration of different cell types in the compound eye. Several putative transcription factors have been identified previously that may be required for expression of genes that specify cell fate in the compound eye. Repression of inappropriate gene expression may be as important as transcriptional activation in the determination of cell fate. We report the identification of a mutation in the Drosophila tramtrack (ttk) locus that is required for cell fate determination in the compound eye. ttk is expressed as two proteins, p69 and p88, shown previously to bind to the regulatory regions of several segmentation genes. In ttk1, an allele missing the mRNA encoding p88, many ommatidia contained supernumerary R7 cells and decreased numbers of R1-R6 cells. ttk1e11, which appears to disrupt both Ttk proteins, was characterized by early embryonic arrest as well as transformation of ommatidial cells into nonommatidial cell types in mosaic flies. Consistent with previous proposals that the Ttk proteins are transcriptional repressors of segmentation genes, we detected ectopic or increased expression of the segment polarity gene engrailed in several ttk1 larval tissues. We propose that p69 is required to repress expression of genes that are incompatible with development of photoreceptor cell fates, whereas p88 appears to be required to repress genes that promote the R7 cell fate.
