Research Article 2309 Yeast ARL1 encodes a regulator of K+ influx Amanda M. Munson, Devon H. Haydon, Sherie L. Love, Gillian L. Fell, Vikram R. Palanivel and Anne G. Rosenwald* Department of Biology, 406 Reiss Science Center, Box 571229, Georgetown University, Washington, DC 20057, USA *Author for correspondence (e-mail:
[email protected]) Accepted 9 December 2003 Journal of Cell Science 117, 2309-2320 Published by The Company of Biologists 2004 doi:10.1242/jcs.01050 Summary A molecular genetic approach was undertaken in regulate K+ import properly, contributing to membrane Saccharomyces cerevisiae to examine the functions of ARL1, hyperpolarity. By contrast, K+ and H+ efflux were encoding a G protein of the Ras superfamily. We show here undisturbed. The loss of ARL1 had no effect on the steady- that ARL1 is an important component of the control of state level or the localization of a tagged version of Trk1p. intracellular K+. The arl1 mutant was sensitive to toxic High copy suppressors of the hygromycin-B phenotype cations, including hygromycin B and other aminoglycoside included SAP155, encoding a protein that interacts with the antibiotics, tetramethylammonium ions, methylammonium cell cycle regulator Sit4p, and HAL4 and HAL5, encoding ions and protons. The hygromycin-B-sensitive phenotype Ser/Thr kinases that regulate the K+-influx mediators was suppressed by the inclusion of K+ and complemented Trk1p and Trk2p. These results are consistent with a model by wild-type ARL1 and an allele of ARL1 predicted to be in which ARL1, via regulation of HAL4/HAL5, governs K+ unbound to nucleotide in vivo. The arl1 mutant strain homeostasis in cells.