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Molecular and Cellular Biology, May 1999, p. 3328-3337, Vol. 19, No. 5
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.
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


*
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.
Present address: PlantTec Biotechnologie GmbH, 14473 Potsdam, Germany.
Present address: Center for Molecular Oncology, University of
Chicago, Chicago, IL 60637-5419.
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