2.7.1.227 physiological function a strain lacking Aur1 activity fails to incorporate inositol or N-acetylsphinganine into sphingolipids and lacks enzyme activity 754050 2.7.1.227 physiological function expression in HEK 293 cells leads to the synthesis of an inositol phosphorylceramide-like species 754074 2.7.1.227 physiological function isoforms IPCS1-3 complement an Aur11 auxotrophic mutant yeast strain and confer aureobasidin A resistance 755041 2.7.1.227 physiological function overexpression of inositol phosphorylceramide synthase isoforms IPCS1, 2 or 3 in Arabidopsis thaliana results in the downregulation of genes involved in plant response to pathogens. In addition, genes associated with the abiotic stress response to salinity, cold and drought are similarly downregulated. The degree of downregulation is specifically correlated with the level of IPCS expression 755186 2.7.1.227 physiological function Saccharomyces cerevisiae transformants harboring AUR1 mutantY166F/G249C are resistant to aureobasidin A 754407 2.7.1.227 physiological function the growth defect of a temperature-sensitive mutant is effectively suppressed by the overexpression of Aur1, and Aur1 and Kei1 proteins form a complex in vivo. The temperature-sensitive mutant is hypersensitive to aureobasidin A, a specific inhibitor of IPC synthesis, and the IPC synthase activity in the mutant membranes is thermolabile. A part of Aur1 is missorted to the vacuole in Kei1 mutant cells. Aur1 without Kei1 has hardly detectable IPC synthase activity 754675 2.7.1.227 physiological function upon downregulation of Aur1 expression, the accumulation of ceramides can lead to cell death. Vesicle-mediated transport between Golgi apparatus, endosomes, and vacuole becomes crucial for survival when Aur1 is repressed, irrespective of the mode of repression. Vacuolar acidification becomes essential when cells are acutely stressed by aureobasidin A. Aureobasidin A activates vacuolar acidification and strongly induces the cell wall integrity pathway 753463