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Molecular and Cellular Biology, November 2008, p. 6646-6657, Vol. 28, No. 21
0270-7306/08/$08.00+0     doi:10.1128/MCB.01162-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Intersection of RNA Processing and the Type II Fatty Acid Synthesis Pathway in Yeast Mitochondria{triangledown}

Melissa S. Schonauer,2 Alexander J. Kastaniotis,3 J. Kalervo Hiltunen,3 and Carol L. Dieckmann1,2*

Department of Biochemistry and Molecular Biophysics,1 Department of Molecular and Cellular Biology, University of Arizona, Tucson, Arizona 85721,2 Biocenter Oulu, Department of Biochemistry, University of Oulu, FI-90014 Oulu, Finland3

Received 22 July 2008/ Returned for modification 19 August 2008/ Accepted 28 August 2008

Distinct metabolic pathways can intersect in ways that allow hierarchical or reciprocal regulation. In a screen of respiration-deficient Saccharomyces cerevisiae gene deletion strains for defects in mitochondrial RNA processing, we found that lack of any enzyme in the mitochondrial fatty acid type II biosynthetic pathway (FAS II) led to inefficient 5' processing of mitochondrial precursor tRNAs by RNase P. In particular, the precursor containing both RNase P RNA (RPM1) and tRNAPro accumulated dramatically. Subsequent Pet127-driven 5' processing of RPM1 was blocked. The FAS II pathway defects resulted in the loss of lipoic acid attachment to subunits of three key mitochondrial enzymes, which suggests that the octanoic acid produced by the pathway is the sole precursor for lipoic acid synthesis and attachment. The protein component of yeast mitochondrial RNase P, Rpm2, is not modified by lipoic acid in the wild-type strain, and it is imported in FAS II mutant strains. Thus, a product of the FAS II pathway is required for RNase P RNA maturation, which positively affects RNase P activity. In addition, a product is required for lipoic acid production, which is needed for the activity of pyruvate dehydrogenase, which feeds acetyl-coenzyme A into the FAS II pathway. These two positive feedback cycles may provide switch-like control of mitochondrial gene expression in response to the metabolic state of the cell.

* Corresponding author. Mailing address: Department of Biochemistry and Molecular Biophysics, P.O. Box 210106, University of Arizona, Tucson, AZ 85721-0106. Phone: (520) 621-3569. Fax: (520) 621-3709. E-mail: dieckman{at}u.arizona.edu

{triangledown} Published ahead of print on 8 September 2008.

Molecular and Cellular Biology, November 2008, p. 6646-6657, Vol. 28, No. 21
0270-7306/08/$08.00+0     doi:10.1128/MCB.01162-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Chen, Z., Kastaniotis, A. J., Miinalainen, I. J., Rajaram, V., Wierenga, R. K., Hiltunen, J. K. (2009). 17{beta}-Hydroxysteroid dehydrogenase type 8 and carbonyl reductase type 4 assemble as a ketoacyl reductase of human mitochondrial FAS. FASEB J. 23: 3682-3691 [Abstract] [Full Text]  
  • Schonauer, M. S., Kastaniotis, A. J., Kursu, V. A. S., Hiltunen, J. K., Dieckmann, C. L. (2009). Lipoic Acid Synthesis and Attachment in Yeast Mitochondria. J. Biol. Chem. 284: 23234-23242 [Abstract] [Full Text]  
  • Hiltunen, J. K., Schonauer, M. S., Autio, K. J., Mittelmeier, T. M., Kastaniotis, A. J., Dieckmann, C. L. (2009). Mitochondrial Fatty Acid Synthesis Type II: More than Just Fatty Acids. J. Biol. Chem. 284: 9011-9015 [Abstract] [Full Text]  


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