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The mutant form of the intracellular asymmetrically localized Numb membrane-bound protein of  Drosophila melanogaster  suppresses the negative complementation of certain  Abruptex  ( Ax ) mutations of the  Notch  ( N ) locus encoding a transmembrane receptor protein in which the  Ax  mutations are mutations in the epidermal growth factor (EGF)-like repeats of the extracellular domain of the receptor. One model for how  Ax  mutants affect  N  function is that they are refractory to an antagonistic signal generated by an excess of  N  ligands. Genetically  numb  ( nb ) is an antagonist of  N . In the absence of  nb,  cells follow the same fate as they would in the presence of a gain-of-function  N  allele, such as  Ax . Numb has been shown to interact with the cytoplasmic domain of Notch. It is therefore suggested that  numb  counteracts the effect of  Abruptex  on Notch ligand binding, i.e. that Numb is an antagonist to the activation of the Notch signal generated by Notch ligands. Numb might accomplish this by interfering with the proteolytic cleavage of the Notch intracellular domain at the cell membrane. Thus, it seems possible that the mechanism of negative complementation of certain  Ax  mutants is the failure of this cleavage. Other possible mechanisms for negative complementation are also discussed.

genetical research

Numb suppresses the negative complementation at the <i>Notch</i> locus of <i>Drosophila melanogaster,</i> suggesting a putative mechanism for negative complementation

Numb suppresses the negative complementation at the Notch locus of Drosophila melanogaster, suggesting a putative mechanism for negative complementation