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First published online 20 October 2004
doi: 10.1242/dev.01448
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1 Department of Biological Science and Technology, Tokyo University of Science,
2641 Yamazaki, Noda, Chiba 278-8510, Japan
2 School of Biological Sciences, University of Manchester, Stopford Building,
Oxford Road, Manchester M13 9PT, UK
3 Department of Nutrition, School of Medicine, University of Tokushima, 3-18-15
Kuramoto, Tokushima 770-8503, Japan
4 Department of Neuroscience and Immunology, Kumamoto University, Graduate
School of Medical Sciences, Honjo 2-2-1, Kumamoto 860-0811, Japan
5 Department of Physiology, Keio University, School of Medicine, 35
Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan
6 Genome and Drug Research Center, Tokyo University of Science, 2641 Yamazaki,
Noda, Chiba 278-8510, Japan
7 PRESTO, JST, 4-1-8 Honcho, Kawaguchi, Saitama, Japan
* Author for correspondence (e-mail: matsuno{at}rs.noda.tus.ac.jp)
Accepted 8 September 2004
Notch (N) signaling is an evolutionarily conserved mechanism that regulates many cell-fate decisions. deltex (dx) encodes an E3-ubiquitin ligase that binds to the intracellular domain of N and positively regulates N signaling. However, the precise mechanism of Dx action is unknown. Here, we found that Dx was required and sufficient to activate the expression of gene targets of the canonical Su(H)-dependent N signaling pathway. Although Dx required N and a cis-acting element that overlaps with the Su(H)-binding site, Dx activated a target enhancer of N signaling, the dorsoventral compartment boundary enhancer of vestigial (vgBE), in a manner that was independent of the Delta (Dl)/Serrate (Ser) ligands- or Su(H). Dx caused N to be moved from the apical cell surface into the late-endosome, where it accumulated stably and co-localized with Dx. Consistent with this, the dx gene was required for the presence of N in the endocytic vesicles. Finally, blocking the N transportation from the plasma membrane to the late-endosome by a dominant-negative form of Rab5 inhibited the Dx-mediated activation of N signaling, suggesting that the accumulation of N in the late-endosome was required for the Dx-mediated Su(H)-independent N signaling.
Key words: Notch signaling, Deltex, Endocytic trafficking, Suppressor of Hairless, Drosophila
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