Yoshida M, Ohnuki S, Yashiroda Y, Ohya Y

A cls5-1 mutant of Saccharomyces cerevisiae is specifically sensitive to high concentrations of Ca(2+), with elevated intracellular calcium content and altered cell morphology in the presence of 100 mM Ca(2+). To reveal the mechanisms of the Ca(2+)-sensitive phenotype, we investigated the gene responsible and its interacting network. We demonstrated that CLS5 ...

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is identical to PFY1, encoding profilin. Involvement of profilin in the maintenance of intracellular Ca(2+) homeostasis was supported by the fact that both exchangeable and non-exchangeable intracellular Ca(2+) pools in the cls5-1 mutant are higher than those of the wild-type strain. Several mutations of the genes whose proteins physically interact with profilin resulted in the Ca(2+)-sensitive phenotype. Examination of the intracellular Ca(2+) pools indicated that Bni1p, Bem1p, Rho1p, and Cla4p are also required for the maintenance of Ca(2+) homeostasis. Quantitative morphological analysis revealed that the Ca(2+)-induced morphological changes in cls5-1 cells are similar to bem1 and cls4-1 cells. Common Ca(2+)-induced morphological changes were an increase in cell size and a decrease of the ratio of budded cells in the population. Since a mutation allele of cls4-1 is located in the CDC24 gene, we suggest that profilin, Bem1p, and Cdc24p are required for Ca(2+)-modulated bud formation. Thus, profilin is involved in Ca(2+) regulation in two ways: the first is Ca(2+) homeostasis by coordination with Bni1p, Bem1p, Rho1p, and Cla4p, and the second is the requirement of Ca(2+) for bud formation by coordination with Bem1p and Cdc24p.

Date: May. 26, 2013

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