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Vol. 16, Issue 10, 4636-4647, October 2005

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The Golgi Ca²⁺-ATPase KlPmr1p Function Is Required for Oxidative Stress Response by Controlling the Expression of the Heat-Shock Element HSP60 in Kluyveromyces lactis

Daniela Uccelletti ^* , Francesca Farina ^* , Paolo Pinton , Paola Goffrini , Patrizia Mancini ^||, Claudio Talora ^||, Rosario Rizzuto , and Claudio Palleschi ^*

^* Department of Developmental and Cell Biology, University of Rome "La Sapienza," 00185 Rome, Italy; Department of Experimental and Diagnostic Medicine, Section of General Pathology, University of Ferrara, 44100 Ferrara, Italy; Department of Genetics, Anthropology, and Evolution, University of Parma, 43100 Parma, Italy; and ^|| Department of Experimental Medicine and Pathology, University of Rome "La Sapienza," 00161 Rome, Italy

Submitted February 17, 2005; Revised July 2, 2005; Accepted July 12, 2005
Monitoring Editor: Jeffrey Brodsky

The Golgi P-type Ca²⁺-ATPase, Pmr1p, is the major player for calcium homeostasis in yeast. The inactivation of KlPMR1 in Kluyveromyces lactis leads to high pleiotropic phenotypes that include reduced glycosylation, cell wall defects, and alterations of mitochondrial metabolism. In this article we found that cells lacking KlPmr1p have a morphologically altered mitochondrial network and that mitochondria (m) from Klpmr1 cells accumulate Ca²⁺ more slowly and reach a lower [Ca²⁺]_m level, when exposed to [Ca²⁺] < 5 µM, than wild-type cells. The Klpmr1 cells also exhibit traits of ongoing oxidative stress and present hyperphosphorylation of KlHog1p, the hallmark for the activation of stress response pathways. The mitochondrial chaperone KlHsp60 acts as a multicopy suppressor of phenotypes that occur in cells lacking the Ca²⁺-ATPase, including relief from oxidative stress and recovery of cell wall thickness and functionality. Inhibition of KlPMR1 function decreases KlHSP60 expression at both mRNA and protein levels. Moreover, KlPRM1 loss of function correlates with both decreases in HSF DNA binding activity and KlHSP60 expression. We suggest a role for KlPMR1 in HSF DNA binding activity, which is required for proper KlHSP60 expression, a key step in oxidative stress response.

These authors contributed equally to this work.

Address correspondence to: Claudio Palleschi (claudio.palleschi{at}uniroma1.it).

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