This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Smith, C. P.
Right arrow Articles by Thorsness, P. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Smith, C. P.
Right arrow Articles by Thorsness, P. E.

 Previous Article  |  Next Article 

Eukaryotic Cell, December 2005, p. 2078-2086, Vol. 4, No. 12
1535-9778/05/$08.00+0     doi:10.1128/EC.4.12.2078-2086.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Formation of an Energized Inner Membrane in Mitochondria with a {gamma}-Deficient F1-ATPase

Christopher P. Smith and Peter E. Thorsness*

Department of Molecular Biology, University of Wyoming, Laramie, Wyoming 82071

Received 4 August 2005/ Accepted 27 September 2005

Eukaryotic cells require mitochondrial compartments for viability. However, the budding yeast Saccharomyces cerevisiae is able to survive when mitochondrial DNA suffers substantial deletions or is completely absent, so long as a sufficient mitochondrial inner membrane potential is generated. In the absence of functional mitochondrial DNA, and consequently a functional electron transport chain and F1Fo-ATPase, the essential electrical potential is maintained by the electrogenic exchange of ATP4– for ADP3– through the adenine nucleotide translocator. An essential aspect of this electrogenic process is the conversion of ATP4– to ADP3– in the mitochondrial matrix, and the nuclear-encoded subunits of F1-ATPase are hypothesized to be required for this process in vivo. Deletion of ATP3, the structural gene for the {gamma} subunit of the F1-ATPase, causes yeast to quantitatively lose mitochondrial DNA and grow extremely slowly, presumably by interfering with the generation of an energized inner membrane. A spontaneous suppressor of this slow-growth phenotype was found to convert a conserved glycine to serine in the ß subunit of F1-ATPase (atp2-227). This mutation allowed substantial ATP hydrolysis by the F1-ATPase even in the absence of the {gamma} subunit, enabling yeast to generate a twofold greater inner membrane potential in response to ATP compared to mitochondria isolated from yeast lacking the {gamma} subunit and containing wild-type ß subunits. Analysis of the suppressing mutation by blue native polyacrylamide gel electrophoresis also revealed that the {alpha}3ß3 heterohexamer can form in the absence of the {gamma} subunit.

* Corresponding author. Mailing address: Department of Molecular Biology, University of Wyoming, Laramie, WY 82071. Phone: (307) 766-2038. Fax: (307) 766-5098. E-mail: thorsnes{at}uwyo.edu.

Eukaryotic Cell, December 2005, p. 2078-2086, Vol. 4, No. 12
1535-9778/05/$08.00+0     doi:10.1128/EC.4.12.2078-2086.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.





Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»