REPRESSION OF DROSOPHILA PHOTORECEPTOR CELL FATE THROUGH COOPERATIVE ACTION OF 2 TRANSCRIPTIONAL REPRESSORS YAN AND TRAMTRACK

The Drosophila yan gene encodes an E twenty-six (ETS) domain nuclear p rotein with a transcription repressor activity that can be downregulat ed through phosphorylation by mitogen-activated protein kinase (MAPK). Before photoreceptor precursor cells commit to a particular cell fate , Yan is required to maintain them in an undifferentiated state. We re port here identification of tramtrack (ttk) mutations that act as domi nant enhancers of yan. We show that ttk synergistically interacts with gan to inhibit the R7 photoreceptor cell fate. Since ttk products are nuclear proteins with zinc-finger DNA-binding motifs, yan and ttk rep resent two nuclear regulators essential for the control of cellular co mpetence for neural differentiation. Reduction of either yan or ttk ac tivity suppresses eye phenotypes of the kinase suppressor of ras (ksr) gene mutation, which is consistent with the involvement of yan and tt k in the Ras/MAPK pathway.