Abstract
A Drosophila gene with similarity to the mammalian Ras GTPase activating protein has been isolated in screens for mutations that affect eye development. Inactivation of the locus, Gap1, mimics constitutive activation of the Sevenless receptor tyrosine kinase and eliminates the need for a functional Sevenless protein in the R7 cell. Our results suggest that Gap1 acts as a negative regulator of signaling by Sevenless by down-regulating the activity of the Ras1 protein, which has been shown to be a key element in signaling by Sevenless.
