Previous Article | Next Article ![]()
Journal of Bacteriology, October 1999, p. 6456-6462, Vol. 181, No. 20
Departamento Bioquímica i Biologia
Molecular,
Received 27 May 1999/Accepted 6 August 1999
Saccharomyces cerevisiae cells lacking the regulatory
subunit of casein kinase 2 (CK-2), encoded by the gene
CKB1, display a phenotype of hypersensitivity to
Na+ and Li+ cations. The sensitivity of a
strain lacking ckb1 is higher than that of a calcineurin
mutant and similar to that of a strain lacking HAL3, the
regulatory subunit of the Ppz1 protein phosphatase. Genetic analysis
indicated that Ckb1 participates in regulatory pathways different from
that of Ppz1 or calcineurin. Deletion of CKB1 increased the
salt sensitivity of a strain lacking Ena1 ATPase, the major determinant
for sodium efflux, suggesting that the function of the kinase is not
mediated by Ena1. Consistently, ckb1 mutants did not show
an altered cation efflux. The function of Ckb1 was independent of the
TRK system, which is responsible for discrimination of
potassium and sodium entry, and in the absence of the kinase regulatory
subunit, the influx of sodium was essentially normal. Therefore, the
salt sensitivity of a ckb1 mutant cannot be attributed to
defects in the fluxes of sodium. In fact, in these cells, both the
intracellular content and the cytoplasm/vacuole ratio for sodium were
similar to those features of wild-type cells. The possible causes for
the salt sensitivity phenotype of casein kinase mutants are discussed
in the light of these findings.
0021-9193/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Biochemical and Genetic Analyses of the Role of
Yeast Casein Kinase 2 in Salt Tolerance
*
Corresponding author. Mailing address: Dept.
Bioquímica i Biologia Molecular, Facultat de Veterinària,
Ed. V, Universitat Autònoma de Barcelona, Bellaterra 08193, Barcelona, Spain. Phone: 34-93-5812182. Fax: 34-93-5812006. E-mail:
J.Arino{at}cc.uab.es.
Journal of Bacteriology, October 1999, p. 6456-6462, Vol. 181, No. 20
0021-9193/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
This article has been cited by other articles:
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»