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Cell-autonomous role of Notch, an epidermal growth factor homologue, in sensory organ differentiation in Drosophila.
Author(s) -
José F. de Celis,
Manuel MaríBeffa,
Antonio Garcı́a-Bellido
Publication year - 1991
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.88.2.632
Subject(s) - biology , microbiology and biotechnology , epidermal growth factor , signal transduction , genetics , notch proteins , cell fate determination , notch signaling pathway , gene , receptor , transcription factor
The gene Notch (N) codes for a transmembrane protein with an extracellular domain that has homologies to epidermal growth factors and an intracellular domain that could be involved in signal transduction. N null alleles cause the transformation of most epidermal cells into neuroblasts in central and peripheral nervous systems. Alleles of the same gene, called Abruptex (Ax), that map to the extracellular domain of N protein cause the absence of adult sensory organs. Both types of alleles show cell autonomy in mosaic analysis carried out in the last stages of the formation of adult sensory organs. The phenotypes are different: cells lacking N gene products differentiate as sensory organ mother cells early and as its neural sublineage later, whereas in the homozygous Ax condition epidermal cells do not enter the sensory organ mother cell pathway. The results indicate that N gene products act internally in the cell, probably as receptors of intercellular signals both in sensory organ mother cell singularization and in fate specification of its daughter cells. Ax mutations behave as an excess of N+ function in this signal transduction process. N proteins modified by these mutations act as constitutively activated.

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