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Ca 2+ ‐ATPase function is required for intracellular trafficking of the Notch receptor in Drosophila
Author(s) -
Periz Goran,
Fortini Mark E.
Publication year - 1999
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/18.21.5983
Subject(s) - biology , endoplasmic reticulum , microbiology and biotechnology , notch proteins , notch signaling pathway , atpase , complementation , transmembrane protein , mutant , membrane protein , transmembrane domain , receptor , gene , biochemistry , signal transduction , enzyme , membrane
Maintaining high Ca 2+ concentrations in the lumen of the endoplasmic reticulum is important for protein synthesis and transport. We identified a lethal complementation group recovered in a screen for mutations that reduce Notch activity as loss‐of‐function alleles of the Drosophila Ca 2+ ‐ATPase gene Ca‐P60A . Analysis of Ca‐P60A mutants indicates that Ca 2+ ‐ATPase is essential for cell viability and tissue morphogenesis during development. Cultured cells treated with Ca 2+ ‐ATPase inhibitors exhibit impaired Notch cleavage and receptor trafficking to the cell surface, explaining the genetic interaction between Ca 2+ ‐ATPase and Notch. Notch and several other transmembrane proteins are mislocalized in tissue clones homozygous for Ca‐P60A mutations, demonstrating a general effect on membrane protein trafficking caused by a deficiency in Ca 2+ ‐ATPase.