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

• DOI: 10.1128/mcb.19.5.3328
• Publication Date: 2015-10-26T10:18:39Z
• Authors: Jose M. Mulet; Martin P. Leube; Stephen J. Kron; Gabino Rios; Gerald R. Fink; Ramon Serrano
• Keywords: 0301 basic medicine; Saccharomyces cerevisiae Proteins; Membrane Proteins; Biological Transport; Saccharomyces cerevisiae; Membrane Potentials; Fungal Proteins; Methylamines; 03 medical and health sciences; Phenotype; Cations; Gene Expression Regulation, Fungal; Mutation; Potassium; Homeostasis; Salts; Cloning, Molecular; Carrier Proteins; Cation Transport Proteins; Protein Kinases

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