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Originally published as Genetics Published Articles Ahead of Print on July 14, 2005.
Genetics, Vol. 171, 517-526, October 2005, Copyright © 2005
doi:10.1534/genetics.105.046540
A Screen for Nigericin-Resistant Yeast Mutants Revealed Genes Controlling Mitochondrial Volume and Mitochondrial Cation Homeostasis
Blanka Kucejova*,
Martin Kucej*,
Silvia Petrezselyova
,
Lenka Abelovska* and
Lubomir Tomaska,1
* Department of Biochemistry, Faculty of Natural Sciences, Comenius University, 84215 Bratislava, Slovak Republic and Department of Genetics, Faculty of Natural Sciences, Comenius University, 84215 Bratislava, Slovak Republic
1 Corresponding author: Department of Genetics, Faculty of Natural Sciences, Comenius University, Mlynska dolina B-1, 84215 Bratislava, Slovak Republic.
E-mail: tomaska{at}fns.uniba.sk
Little is known about the regulation of ion transport across the inner mitochondrial membrane in Saccharomyces cerevisiae. To approach this problem, we devised a screening procedure for facilitating the identification of proteins involved in mitochondrial ion homeostasis. Taking advantage of the growth inhibition of yeast cells by electroneutral K+/H+ ionophore nigericin, we screened for genetic mutations that would render cells tolerant to this drug when grown on a nonfermentable carbon source and identified several candidate genes including MDM31, MDM32, NDI1, YMR088C (VBA1), CSR2, RSA1, YLR024C, and YNL136W (EAF7). Direct examination of intact cells by electron microscopy indicated that mutants lacking MDM31 and/or MDM32 genes contain dramatically enlarged, spherical mitochondria and that these morphological abnormalities can be alleviated by nigericin. Mitochondria isolated from the 
mdm31 and mdm32 mutants exhibited limited swelling in an isotonic solution of potassium acetate even in the presence of an exogenous K+/H+ antiport. In addition, growth of the mutants was inhibited on ethanol-containing media in the presence of high concentrations of salts (KCl, NaCl, or MgSO4) and their mitochondria exhibited two- (mdm31 and mdm32) to threefold (mdm31mdm32) elevation in magnesium content. Taken together, these data indicate that Mdm31p and Mdm32p control mitochondrial morphology through regulation of mitochondrial cation homeostasis and the maintenance of proper matrix osmolarity.
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