Integrative genomics identifies MCU as an essential component of the mitochondrial calcium uniporter (original) (raw)
- Letter
- Published: 19 June 2011
- Fabiana Perocchi1,2 na1,
- Hany S. Girgis1,2,
- Molly Plovanich1,2,
- Casey A. Belcher-Timme1,2,
- Yasemin Sancak1,2,
- X. Robert Bao1,2,
- Laura Strittmatter1,2,
- Olga Goldberger1,2,
- Roman L. Bogorad3,
- Victor Koteliansky4 &
- …
- Vamsi K. Mootha1,2
Nature volume 476, pages 341–345 (2011)Cite this article
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Abstract
Mitochondria from diverse organisms are capable of transporting large amounts of Ca2+ via a ruthenium-red-sensitive, membrane-potential-dependent mechanism called the uniporter1,2,3,4. Although the uniporter’s biophysical properties have been studied extensively, its molecular composition remains elusive. We recently used comparative proteomics to identify MICU1 (also known as CBARA1), an EF-hand-containing protein that serves as a putative regulator of the uniporter5. Here, we use whole-genome phylogenetic profiling, genome-wide RNA co-expression analysis and organelle-wide protein coexpression analysis to predict proteins functionally related to MICU1. All three methods converge on a novel predicted transmembrane protein, CCDC109A, that we now call ‘mitochondrial calcium uniporter’ (MCU). MCU forms oligomers in the mitochondrial inner membrane, physically interacts with MICU1, and resides within a large molecular weight complex. Silencing MCU in cultured cells or in vivo in mouse liver severely abrogates mitochondrial Ca2+ uptake, whereas mitochondrial respiration and membrane potential remain fully intact. MCU has two predicted transmembrane helices, which are separated by a highly conserved linker facing the intermembrane space. Acidic residues in this linker are required for its full activity. However, an S259A point mutation retains function but confers resistance to Ru360, the most potent inhibitor of the uniporter. Our genomic, physiological, biochemical and pharmacological data firmly establish MCU as an essential component of the mitochondrial Ca2+ uniporter.
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Acknowledgements
We thank R. Nilsson, J. Engreitz and S. Calvo for bioinformatics assistance; D. Root and S. Silver for assistance in lentiviral RNAi; B. R. Bettencourt, K. Charisse, S. Kuchimanchi and L. Speciner for siRNA design, synthesis and formulation; M. Blower, J. Avruch and R. Ward for advice; and members of the Mootha laboratory for valuable feedback. J.M.B. and L.S. were supported by graduate student fellowships from the National Science Foundation. This work was supported by grants from the National Institutes of Health (GM0077465, DK080261) awarded to V.K.M.
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- Joshua M. Baughman and Fabiana Perocchi: These authors contributed equally to this work.
Authors and Affiliations
- Departments of Systems Biology and Medicine, Harvard Medical School and Massachusetts General Hospital, Boston, 02114, Massachusetts, USA
Joshua M. Baughman, Fabiana Perocchi, Hany S. Girgis, Molly Plovanich, Casey A. Belcher-Timme, Yasemin Sancak, X. Robert Bao, Laura Strittmatter, Olga Goldberger & Vamsi K. Mootha - Broad Institute, Cambridge, 02142, Massachusetts, USA
Joshua M. Baughman, Fabiana Perocchi, Hany S. Girgis, Molly Plovanich, Casey A. Belcher-Timme, Yasemin Sancak, X. Robert Bao, Laura Strittmatter, Olga Goldberger & Vamsi K. Mootha - Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, 02139, Massachusetts, USA
Roman L. Bogorad - Alnylam Pharmaceuticals, Inc., Cambridge, 02142, Massachusetts, USA
Victor Koteliansky
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Contributions
J.M.B., F.P. and V.K.M. conceived of the project and its design. J.M.B., F.P., H.S.G., M.P., O.G., L.S., C.A.B.-T., X.R.B., Y.S. and R.L.B. performed experiments and data analysis. V.K. aided in experimental design. V.K.M., J.M.B., F.P. and M.P. wrote the manuscript.
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Correspondence toVamsi K. Mootha.
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Baughman, J., Perocchi, F., Girgis, H. et al. Integrative genomics identifies MCU as an essential component of the mitochondrial calcium uniporter.Nature 476, 341–345 (2011). https://doi.org/10.1038/nature10234
- Received: 09 November 2010
- Accepted: 02 June 2011
- Published: 19 June 2011
- Issue Date: 18 August 2011
- DOI: https://doi.org/10.1038/nature10234
Editorial Summary
Mitochondrial Ca2+ channel identified
Central to the role of the mitochondrion in cellular metabolism is its ability to control the fluxes of the key signalling ion, Ca2+. This is done by a highly selective ion channel known as the mitochondrial calcium uniporter. The molecular nature of this channel has remained elusive, but now two groups report the identification of a 40-kilodalton protein in the inner membrane of mitochondria as the active channel of the uniporter. This protein contains two transmembrane domains and exhibits calcium-channel activity in vitro and in vivo.