The intracellular deletions of DELTA and SERRATE define dominant negative forms of the Drosophila Notch ligands (original) (raw)
RESEARCH ARTICLE| 01 August 1996
Howard Hughes Medical Institute and Department of Cell Biology and Biology, Boyer Center for Molecular Medicine, Yale University, 295 Congress Avenue, New Haven, Connecticut 06536-0812, USA
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Spyros Artavanis-Tsakonas
Howard Hughes Medical Institute and Department of Cell Biology and Biology, Boyer Center for Molecular Medicine, Yale University, 295 Congress Avenue, New Haven, Connecticut 06536-0812, USA
Search for other works by this author on:
Xin Sun
Howard Hughes Medical Institute and Department of Cell Biology and Biology, Boyer Center for Molecular Medicine, Yale University, 295 Congress Avenue, New Haven, Connecticut 06536-0812, USA
Spyros Artavanis-Tsakonas
Howard Hughes Medical Institute and Department of Cell Biology and Biology, Boyer Center for Molecular Medicine, Yale University, 295 Congress Avenue, New Haven, Connecticut 06536-0812, USA
Online ISSN: 1477-9129
Print ISSN: 0950-1991
© 1996 by Company of Biologists
1996
Development (1996) 122 (8): 2465–2474.
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ABSTRACT
We examined the function of the intracellular domains of the two known Drosophila Notch ligands, Delta and Serrate, by expressing wild-type and mutant forms in the developing Drosophila eye under the sevenless promoter. The expression of intracellularly truncated forms of either Delta (sev-DlTM) or Serrate (sev-SerTM) leads to extra photoreceptor phenotypes, similar to the eye phenotypes associated with loss-of-function mutations of either Notch or Delta. Consistent with the notion that the truncated ligands reduce Notch signalling activity, the eye phenotypes of sevDlTM and sev-SerTM are enhanced by loss-of-function mutations in the Notch pathway elements, Notch, Delta, mastermind, deltex and groucho, but are suppressed by a duplication of Delta or mutations in Hairless, a negative regulator of the pathway. These observations were extended to the molecular level by demonstrating that the expression of _Enhancer of split m_δ, a target of Notch signalling, is down-regulated by the truncated ligands highly expressed in neighbouring cells. We conclude that the truncated ligands act as antagonists of Notch signalling.
© 1996 by Company of Biologists
1996
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