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. Author manuscript; available in PMC: 2014 Sep 1.
Published in final edited form as: Wiley Interdiscip Rev Dev Biol. 2013 Feb 11;2(5):701–721. doi: 10.1002/wdev.111

Figure 5. The N pathway and signaling during early neurogenesis.

Figure 5

(A) Core elements of the N pathway (AS-C, transcripts of AS-C; E(spl), transcripts of E(spl)-C; Nicd, cleaved intracellular domain of N). (B) Three types of Notch signaling (lateral inhibition, inductive signaling, mitosis-associated Notch inhibition). Rectangles represent neurectoderm; red shading indicates potential cell fate. In lateral inhibition, all cells start out with a neurogenic fate (left); Notch-mediated lateral inhibition restricts neural fate to NBs (center); loss of Notch results in neural hyperplasia (right). Inductive signaling presupposes a population of cells that are already committed to a specific fate (e.g., wing margin; photoreceptors; left panel). These cells send a N signal to their neighbors inducing in them the expression of other fate determinants (center). Loss of N results in the failure of induction, often accompanied by cell death (right). The signaling scenario at the bottom links N signaling to cell division: prior to mitosis, N pathway is active in all cells (e.g. NBs; SOPs; left); at the same time, the N inhibitor Numb (purple) is channeled into one daughter cell, which thereupon shuts off the N pathway and adopts a different fate (center); loss of N results in both cells retaining their original fate (right). (C) Modulators and signal transducers of the N pathway.