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A more recent version of this article appeared on November 22, 2000
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Papers In Press, published online ahead of print September 8, 2000
J. Biol. Chem, 10.1074/jbc.M007338200
Submitted on August 11, 2000
Revised on September 7, 2000
Accepted on September 8, 2000

Multiple signals from dysfunctional mitochondria activate the pleiotropic drug resistance pathway in saccharomyces cerevisiae

Timothy C. Hallstrom and W. Scott Moye-Rowley

Department of Physiology and Biophysics, University of Iowa, Iowa City, IA 52242

Corresponding Author: moyerowl{at}blue.weeg.uiowa.edu

Multiple or pleiotropic drug resistance most often occurs in Saccharomyces cerevisiae due to substitution mutations within the Cys6-Zn(II) transcription factors Pdr1p and Pdr3p. These dominant transcriptional regulatory proteins cause elevated drug resistance and overexpression of the ATP-binding cassette transporter-encoding gene, PDR5. We have carried out a genetic screen to identify negative regulators of PDR5 expression and found that loss of the mitochondrial genome (rho 0 cells) causes up-regulation of Pdr3p but not Pdr1p function. Additionally, loss of the mitochondrial inner membrane protein Oxa1p generates a signal that results in increased Pdr3p activity. Both of these mitochondrial defects lead to increased expression of the PDR3 structural gene. Importantly, the signaling pathway used to enhance Pdr3p function in rho 0 cells is not the same as in oxa1 cells. Loss of previously described nuclear-mitochondrial signaling genes like RTG1 reduce the level of PDR5 expression and drug resistance seen in rho 0 cells but has no effect on oxa1-induced phenotypes. These data uncover a new regulatory pathway connecting expression of multidrug resistance genes with mitochondrial function.


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