Nagel A C, Preiss A
Institut für Genetik (240), Universität Hohenheim, Garbenstrasse 30, Stuttgart, 70599, Germany.
Dev Biol. 1999 Apr 15;208(2):406-15. doi: 10.1006/dbio.1999.9203.
Eye development in Drosophila involves the Notch signaling pathway at several consecutive steps. At first, Notch signaling is required for stable expression of the proneural gene atonal (ato), thereby maintaining neural potential of the cells. Second, in a process of lateral inhibition, Notch signaling is necessary to confine neural commitment to individual photoreceptor founder cells. Later on, the successive addition of cells to maturing ommatidia is under Notch control. In contrast to previous assumptions, the recessive Notch allele split (Nspl) involves specifically loss of the early proneural Notch activity in the eye, which is in agreement with bristle defects as well. As a result, fewer cells gain neural potential and fewer ommatidia are founded. Enhancement of this phenotype by the dominant mutation Enhancer of split [E(spl)D] happens within the remaining proneural cells, in which Ato expression is abolished. In line with genetic data, this process occurs primarily at the protein level due to altered protein-protein interactions between the aberrant E(spl)D and proneural proteins. Nspl is the first Notch mutation known to specifically affect Notch inductive processes during eye development.
果蝇的眼睛发育在几个连续步骤中涉及Notch信号通路。首先，Notch信号通路对于原神经基因无调性（ato）的稳定表达是必需的，从而维持细胞的神经潜能。其次，在侧向抑制过程中，Notch信号通路对于将神经分化限制在单个感光细胞前体细胞是必要的。后来，向成熟小眼连续添加细胞受Notch信号通路控制。与先前的假设相反，隐性Notch等位基因分裂（Nspl）特别涉及眼睛中早期原神经Notch活性的丧失，这也与刚毛缺陷一致。结果，获得神经潜能的细胞减少，形成的小眼也减少。显性突变分裂增强子[E(spl)D]对这种表型的增强发生在剩余的原神经细胞中，其中Ato表达被消除。与遗传数据一致，由于异常的E(spl)D与原神经蛋白之间蛋白质 - 蛋白质相互作用的改变，这个过程主要发生在蛋白质水平。Nspl是已知的第一个在眼睛发育过程中特异性影响Notch诱导过程的Notch突变。
