A 122-bp Eye-Specific yan Enhancer Mediates Crosstalk between Notch/Su(H) and RTK/Pointed Signaling. M.C. Rohrbaugh ¹, E. Ramos ², D. Nguyen ³, M. Price ³, Y. Wen ³, Z.C. Lai ^1,2,3. 1) Department of Biochemistry, Microbiology and Molecular Biology,; 2) Intercollege Program in Genetics,; 3) Department of Biology, Pennsylvania State University, University Park, PA.

   During Drosophila eye development, one of the functions mediated by Notch signaling is to restrict cellular competence for differentiation. Contrary to this, the RTK pathway provides inductive signals for the recruitment of photoreceptors into developing ommatidia. How these two pathways oppose each other during differentiation is not clearly understood. A possible answer to this question lies in the transcriptional regulation of the yan gene. Yan, a general inhibitor of neuronal differentiation, is required to maintain cells in a precursor state prior to ommatidium recruitment. In our studies, we have isolated an eye-specific 122-bp enhancer of the yan gene. We found that Notch and a critical component of the Notch pathway, Su(H), are essential for reporter gene transcription via this 122-bp enhancer as well as endogenous Yan expression. This activation is disrupted by members of the RTK pathway. One such member, Pointed, is also able to directly bind to the yan enhancer and compete with Su(H) for DNA binding. Thus, the yan enhancer provides a point where Notch and RTK pathways intersect in an opposing manner.