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  MOF Acetyl Transferase Regulates Transcription and Respiration in Mitochondria

Chatterjee, A., Seyfferth, J., Lucci, J., Glisbach, R., Preissl, S., Böttinger, L., et al. (2016). MOF Acetyl Transferase Regulates Transcription and Respiration in Mitochondria. Cell, 167, 722-738. doi:10.1016/j.cell.2016.09.052.

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Chatterjee, Aindrilla1, Author
Seyfferth, Janine1, Author
Lucci, Jacopo1, Author
Glisbach, Ralf2, Author
Preissl, Sebastian2, Author
Böttinger, Lena2, Author
Martensson, Christoph U.2, Author
Panhale, Amol1, Author
Stehle, Thomas1, Author
Kretz, Oliver2, Author
Sahyoun, Abdullah H.3, Author
Avilov, Sergiy3, Author              
Eimer, Stefan2, Author
Hein, Lutz2, Author
Pfanner, Nicolaus2, Author
Becker, Thomas2, Author
Akhtar, Asifa1, Author              
Affiliations:
1Department of Chromatin Regulation, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243643              
2External Organizations, ou_persistent22              
3Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243641              

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 Abstract: A functional crosstalk between epigenetic regulators and metabolic control could provide a mechanism to adapt cellular responses to environmental cues. We report that the well-known nuclear MYST family acetyl transferase MOF and a subset of its non-specific lethal complex partners reside in mitochondria. MOF regulates oxidative phosphorylation by controlling expression of respiratory genes from both nuclear and mtDNA in aerobically respiring cells. MOF binds mtDNA, and this binding is dependent on KANSL3. The mitochondrial pool of MOF, but not a catalytically deficient mutant, rescues respiratory and mtDNA transcriptional defects triggered by the absence of MOF. Mof conditional knockout has catastrophic consequences for tissues with high-energy consumption, triggering hypertrophic cardiomyopathy and cardiac failure in murine hearts; cardiomyocytes show severe mitochondrial degeneration and deregulation of mitochondrial nutrient metabolism and oxidative phosphorylation pathways. Thus, MOF is a dual-transcriptional regulator of nuclear and mitochondrial genomes connecting epigenetics and metabolism.

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Language(s): eng - English
 Dates: 2016-10-20
 Publication Status: Published online
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 Rev. Type: Peer
 Identifiers: DOI: 10.1016/j.cell.2016.09.052
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Title: Cell
Source Genre: Journal
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Publ. Info: Cambridge, Mass. : Cell Press
Pages: - Volume / Issue: 167 Sequence Number: - Start / End Page: 722 - 738 Identifier: ISSN: 0092-8674
CoNE: https://pure.mpg.de/cone/journals/resource/954925463183