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Published July 1997 | public
Journal Article

Fringe boundaries coincide with Notch-dependent patterning centres in mammals and alter Notch-dependent development in Drosophila

Abstract

In both vertebrate and invertebrate development, cells are often programmed to adopt fates distinct from their neighbors. Genetic analyses in Drosophila melanogaster have highlighted the importance of cell surface and secreted proteins in these cell fate decisions. Homologues of these proteins have been identified and shown to play similar roles in vertebrate development. Fringe, a novel signalling protein, has been shown to induce wing margin formation in Drosophila. Fringe shares significant sequence homology and predicted secondary structure similarity with bacterial glycosyltransferases. Thus, fringe may control wing development by altering glycosylation of cell surface and/or secreted molecules. Recently, two fringe genes were isolated from Xenopus laevis. We report here the cloning and characterization of three murine fringe genes (lunatic fringe, manic fringe and radical fringe). We find in several tissues that fringe expression boundaries coincide with Notch-dependent patterning centres and with Notch-ligand expression boundaries. Ectopic expression of murine manic fringe or radical fringe in Drosophila results in phenotypes that resemble those seen in Notch mutants.

Additional Information

© 1997 Nature Publishing Group. Received 28 February; Accepted 28 May 1997. We thank K. Irvine, T. Vogt, E. Laufer and R. Fleming for exchange of information and H.X. Cheng, along with ACGT and the Centres of Excellence sequencing facility, for DNA sequencing. We are also indebted to K. Irvine, H. Krause and the Bloomington stock center for Drosophila stocks. Finally, we thank S. Cohen, W. Fu, A. Karaiskakis, T. Yager, ]. Rossant, M. Crackower, D. Van der Kooy, E. Zacksenhaus, H. Schachter, members of our labs, C. Kintner, Yi Rao and many other collegues either for advice, help, information or encouragement. C. C. is a research fellow of the National Cancer Institute of Canada. This work was supported by grants to S.E.E. from the Medical Research Council of Canada, to H. D.L. from the National Science Foundation (USA) and the Medical Research Council of Canada, to R.A.P. from The National Cancer Institute of Canada with funds from the Canadian Cancer Society, to B. G. from the National Cancer Institute of Canada with funds from the Terry Fox Run, to C.C.H. from the National Cancer Institute of Canada with funds from the Terry Fox Run and to G.B. from the Medical Research Council of Canada.

Additional details

Created:
August 19, 2023
Modified:
October 23, 2023