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Molecular and Cellular Biology, May 1999, p. 3328-3337, Vol. 19, No. 5
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

A Novel Mechanism of Ion Homeostasis and Salt Tolerance in Yeast: the Hal4 and Hal5 Protein Kinases Modulate the Trk1-Trk2 Potassium Transporter

Jose M. Mulet,1 Martin P. Leube,1,dagger Stephen J. Kron,2,Dagger Gabino Rios,1 Gerald R. Fink,2 and Ramon Serrano1,*

Instituto de Biologia Molecular y Celular de Plantas, Universidad Politecnica de Valencia-C.S.I.C., 46022 Valencia, Spain,1 and Whitehead Institute for Biomedical Research, Cambridge, Massachusetts 02142-14792

Received 20 November 1998/Returned for modification 22 December 1998/Accepted 28 January 1999

The regulation of intracellular ion concentrations is a fundamental property of living cells. Although many ion transporters have been identified, the systems that modulate their activity remain largely unknown. We have characterized two partially redundant genes from Saccharomyces cerevisiae, HAL4/SAT4 and HAL5, that encode homologous protein kinases implicated in the regulation of cation uptake. Overexpression of these genes increases the tolerance of yeast cells to sodium and lithium, whereas gene disruptions result in greater cation sensitivity. These phenotypic effects of the mutations correlate with changes in cation uptake and are dependent on a functional Trk1-Trk2 potassium transport system. In addition, hal4 hal5 and trk1 trk2 mutants exhibit similar phenotypes: (i) they are deficient in potassium uptake; (ii) their growth is sensitive to a variety of toxic cations, including lithium, sodium, calcium, tetramethylammonium, hygromycin B, and low pH; and (iii) they exhibit increased uptake of methylammonium, an indicator of membrane potential. These results suggest that the Hal4 and Hal5 protein kinases activate the Trk1-Trk2 potassium transporter, increasing the influx of potassium and decreasing the membrane potential. The resulting loss in electrical driving force reduces the uptake of toxic cations and improves salt tolerance. Our data support a role for regulation of membrane potential in adaptation to salt stress that is mediated by the Hal4 and Hal5 kinases.

* Corresponding author. Mailing address: Instituto de Biologia Molecular y Celular de Plantas, Universidad Politecnica de Valencia-C.S.I.C., Camino de Vera s/n, 46022 Valencia, Spain. Phone: 34-96-3877860. Fax: 34-96-3877859. E-mail: serrano{at}ibmcp.upv.es.

dagger Present address: PlantTec Biotechnologie GmbH, 14473 Potsdam, Germany.

Dagger Present address: Center for Molecular Oncology, University of Chicago, Chicago, IL 60637-5419.

Molecular and Cellular Biology, May 1999, p. 3328-3337, Vol. 19, No. 5
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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