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Sanpodo: a context-dependent activator and inhibitor of Notch signaling during asymmetric divisions.

Authors
  • Babaoglan, A Burcu
  • O'Connor-Giles, Kate M
  • Mistry, Hemlata
  • Schickedanz, Adam
  • Wilson, Beth A
  • Skeath, James B
Type
Published Article
Journal
Development
Publisher
The Company of Biologists
Publication Date
Dec 01, 2009
Volume
136
Issue
24
Pages
4089–4098
Identifiers
DOI: 10.1242/dev.040386
PMID: 19906847
Source
Medline
License
Unknown

Abstract

Asymmetric cell divisions generate sibling cells of distinct fates ('A', 'B') and constitute a fundamental mechanism that creates cell-type diversity in multicellular organisms. Antagonistic interactions between the Notch pathway and the intrinsic cell-fate determinant Numb appear to regulate asymmetric divisions in flies and vertebrates. During these divisions, productive Notch signaling requires sanpodo, which encodes a novel transmembrane protein. Here, we demonstrate that Drosophila sanpodo plays a dual role to regulate Notch signaling during asymmetric divisions - amplifying Notch signaling in the absence of Numb in the 'A' daughter cell and inhibiting Notch signaling in the presence of Numb in the 'B' daughter cell. In so doing, sanpodo ensures the asymmetry in Notch signaling levels necessary for the acquisition of distinct fates by the two daughter cells. These findings answer long-standing questions about the restricted ability of Numb and Sanpodo to inhibit and to promote, respectively, Notch signaling during asymmetric divisions.

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