Fringe forms a complex with Notch

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The Fringe protein of Drosophila and its vertebrate homologues function in boundary determination during pattern formation(1-9). Fringe has been proposed to inhibit Serrate-Notch signalling but to potentiate Delta-Notch signalling(10). Here we show that Fringe and Notch form a complex through both the Lin-Notch repeats and the epidermal growth factor repeats 22-36 (EGF22-36) of Notch when they are co-expressed. The Abruptex(59b) (Ax(59b)) and Ax(M1) mutations, which are caused by missense mutations in EGF repeats 24 and 25, respectively, abolish the Fringe-Notch interaction through EGF22-36, whereas the l(1)N-B mutation in the third Lin-Notch repeat of Notch abolishes the interaction through Lin-Notch repeats. Ax mutations also greatly affect the Notch response to ectopic Fringe in vivo. Results from in vitro protein mixing experiments and subcellular colocalization experiments indicate that the Fringe-Notch complex may form before their secretion. These findings explain how Fringe acts cell-autonomously to modulate the ligand preference of Notch and why the Fringe-Notch relationship is conserved between phyla and in the development of very diverse structures.
Publisher
Nature Publishing Group
Issue Date
2000-01
Language
English
Article Type
Article
Keywords

DROSOPHILA WING DEVELOPMENT; DORSAL-VENTRAL BOUNDARY; DORSOVENTRAL BOUNDARY; SIGNAL-TRANSDUCTION; EXPRESSION; ACTIVATION; RECEPTOR; SERRATE; GROWTH; DELTA

Citation

NATURE, v.405, no.1, pp.191 - 195

ISSN
0028-0836
DOI
10.1038/35012090
URI
http://hdl.handle.net/10203/72440
Appears in Collection
BS-Journal Papers(저널논문)
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