The Drosophila yan gene encodes an E twenty-six (ETS) domain nuclear protein with a transcription repressor activity that can be downregulated 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 report here identification of tramtrack (ttk) mutations that act as dominant enhancers of yan. We show that ttk synergistically interacts with yan to inhibit the R7 photoreceptor cell fate. Since ttk products are nuclear proteins with zinc- finger DNA-binding motifs, yah and ttk represent two nuclear regulators essential for the control of cellular competence for neural differentiation. Reduction of either yah or ttk activity suppresses eye phenotypes of the kinase suppressor of ras (ksr) gene mutation, which is consistent with the involvement of yah and ttk in the Ras/MAPK pathway.
|Original language||English (US)|
|Number of pages||7|
|State||Published - Nov 1 1997|
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