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Abstract

In this report, a glycogen synthase kinase-3 homolog, RIM11, was isolated in a multicopy screen for suppressors of the salt-sensitive phenotype of casein kinase II (CKII) regulatory subunit mutants. Previously known as a gene involved in regulating the initiation of meiosis, RIM11 is now characterized as a determinant of salt-tolerance in cells growing on media containing galactose as the primary carbon source. Consistent with this, rim11 .mutants are shown to be salt-sensitive on galactose media, but not on glucose media. The salt-sensitivity of rim11 .mutants is found to be additive with that of CKII mutants, suggesting that the Rim11 and CKII kinases do not operate in the same biochemical pathway. RIM11 overexpression is found to improve the salt-tolerance of the wild-type strain, as well as CKII and calcineurin mutants, and the catalytic activity of Rim11 is determined to be necessary for this effect. Finally, Rim11 protein levels are shown to be higher when cells are grown on galactose-containing compared to glucose-containing media, and also to be induced upon exposure to NaCl. RIM11 is proposed to be a galactose-specific determinant of salt-tolerance in Saccharomyces cerevisiae.

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