Drosophila deltex mediates suppressor of hairless-independent and late-endosomal activation of notch signaling

Kazuya Hori, Maggy Fostier, Mikiko Ito, Takashi J. Fuwa, Masahiro J. Go, Hideyuki Okano, Martin Baron, Kenji Matsuno

Research output: Contribution to journalArticlepeer-review

167 Citations (Scopus)


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 (DI)/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.

Original languageEnglish
Pages (from-to)5527-5537
Number of pages11
Issue number22
Publication statusPublished - 2004 Nov


  • Deltex
  • Drosophila
  • Endocytic trafficking
  • Notch signaling
  • Suppressor of hairless

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology


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