Notch(spl) is deficient for inductive processes in the eye, and E(spl)(D) enhances split by interfering with proneural activity

Eye development in Drosophila involves the Notch signaling pathway at sever al consecutive steps. At first, Notch signaling is required for stable expr ession of the proneural gene atonal (ato), thereby maintaining neural poten tial of the cells. Second, in a process of lateral inhibition, Notch signal ing is necessary to confine neural commitment to individual photoreceptor f ounder cells. Later on, the successive addition of cells to maturing ommati dia is under Notch control. Zn contrast to previous assumptions, the recess ive Notch allele split (N-spl) involves specifically loss of the early pron eural Notch activity in the eye, which is in agreement with bristle defects as well. As a result, fewer cells gain neural potential and fewer ommatidi a are founded. Enhancement of this phenotype by the dominant mutation Enhan cer of split [E(spl)(D)] happens within the remaining proneural cells, in w hich Ato expression is abolished. In line with genetic data, this process o ccurs primarily at the protein level due to altered protein-protein interac tions between the aberrant E(spl)(D) and proneural proteins. N-spl is the f irst Notch mutation known to specifically affect Notch inductive processes during eye development. (C) 1999 Academic Press.