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Suppression of a Defect in Mitochondrial Protein Import Identifies Cytosolic Proteins Required for Viability of Yeast Cells Lacking Mitochondrial DNA
Cory D. Dunna and Robert E. Jensenaa Department of Cell Biology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205
Corresponding author: Robert E. Jensen, The Johns Hopkins University School of Medicine, 725 N. Wolfe St., Baltimore, MD 21205., rjensen{at}jhmi.edu (E-mail)
Communicating editor: A. P. MITCHELL
mutants to live without mitochondrial DNA (mtDNA). We identified several genes encoding cytosolic proteins, including CCT6, SSB1, ICY1, TIP41, and PBP1, which, when overproduced, rescue the mtDNA dependence of tim18 cells. Furthermore, these same plasmids rescue the petite-negative phenotype of cells lacking other components of the mitochondrial protein import machinery. Strikingly, disruption of the genes identified by the different suppressors produces cells that are unable to grow without mtDNA. We speculate that loss of mtDNA leads to a lowered inner membrane potential, and subtle changes in import efficiency can no longer be tolerated. Our results suggest that increased amounts of Cct6p, Ssb1p, Icy1p, Tip41p, and Pbp1p help overcome the problems resulting from a defect in protein import.
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