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Please use this identifier to cite or link to this item: https://hdl.handle.net/2445/43201
Mitochondrial fusion is increased by the nuclear coactivator PGC-1beta
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Background There is no evidence to date on whether transcriptional regulators are able to shift the balance between mitochondrial fusion and fission events through selective control of gene expression. Methodology/Principal Findings Here, we demonstrate that reduced mitochondrial size observed in knock-out mice for the transcriptional regulator PGC-1β is associated with a selective reduction in Mitofusin 2 (Mfn2) expression, a mitochondrial fusion protein. This decrease in Mfn2 is specific since expression of the remaining components of mitochondrial fusion and fission machinery were not affected. Furthermore, PGC-1β increases mitochondrial fusion and elongates mitochondrial tubules. This PGC-1β-induced elongation specifically requires Mfn2 as this process is absent in Mfn2-ablated cells. Finally, we show that PGC-1β increases Mfn2 promoter activity and transcription by coactivating the nuclear receptor Estrogen Related Receptor α (ERRα). Conclusions/Significance Taken together, our data reveal a novel mechanism by which mammalian cells control mitochondrial fusion. In addition, we describe a novel role of PGC-1β in mitochondrial physiology, namely the control of mitochondrial fusion mainly through Mfn2.
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LIESA TORRE-MARÍN, Montserrat, et al. Mitochondrial fusion is increased by the nuclear coactivator PGC-1beta. PLoS One. 2008. Vol. 3, num. 10, pags. e3613. ISSN 1932-6203. [consulted: 18 of June of 2026]. Available at: https://hdl.handle.net/2445/43201