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J. Biol. Chem., Vol. 280, Issue 50, 41366-41372, December 16, 2005

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The Structural and Functional Role of Med5 in the Yeast Mediator Tail Module^*

Jenny Béve, Guo-Zhen Hu¶||, Lawrence C. Myers, Darius Balciunas¶||1, Olivera Werngren, Kjell Hultenby**, Rolf Wibom, Hans Ronne¶||, and Claes M. Gustafsson2

From the Division of Metabolic Diseases and ^**Clinical Research Center, Karolinska Institutet, Novum, Karolinska University Hospital, SE-141 86 Stockholm, Sweden, the ^¶Department of Medical Biochemistry and Microbiology, Uppsala University, Box 582, SE-751 23 Uppsala, Sweden, the ^||Department of Plant Biology and Forest Genetics, Uppsala Genetic Center, Swedish University of Agricultural Sciences, Box 7080, SE-750 07 Uppsala, Sweden, and the Department of Biochemistry, Dartmouth Medical School, Hanover, New Hampshire 03755-3844

Med5 (Nut1) is identified here as a component of the Mediator tail region. Med5 is positioned peripherally to Med16 (Sin4) together with the three members of the putative Gal11 module, Med15 (Gal11), Med2, and Med3 (Pgd1). The biochemical analysis receives support from genetic interactions between med5 and med15 deletions. The med5 and med16 deletion strains share many phenotypes, including effects on mitochondrial function with enhanced growth on nonfermentable carbon sources, increased citrate synthase activity, and increased oxygen consumption. Deletion of the MED5 gene leads to increased transcription of nuclear genes encoding components of the oxidative phosphorylation machinery, whereas mitochondrial genes encoding components of the same machinery are down-regulated. We discuss a possible role for Med5 in coordinating nuclear and mitochondrial gene transcription.

Received for publication, October 13, 2005

^* This work was supported by grants from the Swedish Cancer Society (to C. M. G.), the Swedish Research Council (to H. R. and C. M. G.), the Swedish Foundation for Strategic Research (to C. M. G.), the European Commission (fp6 EUMITOCOMBAT) (to C. M. G.), and the Erik and Mai Pehrsson Foundation (to H. R.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ Current address: Dept. of Genetics, Cell Biology, and Development, University of Minnesota, 6-160 Jackson Hall, 321 Church St. S.E., Minneapolis, MN 55455.

² To whom correspondence should be addressed: Karolinska Institute, Division of Metabolic Diseases, Novum, SE-141 86 Stockholm, Sweden, Tel.: 46-8-585-83974; Fax: 46-8-779-5383; E-mail: claes.gustafsson{at}ki.se.

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