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MOF Acetyl Transferase Regulates Transcription and Respiration in Mitochondria

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MOF Acetyl Transferase Regulates Transcription and Respiration in Mitochondria. / Chatterjee, Aindrila; Seyfferth, Janine; Lucci, Jacopo; Gilsbach, Ralf; Preissl, Sebastian; Böttinger, Lena; Mårtensson, Christoph U; Panhale, Amol; Stehle, Thomas; Kretz, Oliver; Sahyoun, Abdullah H; Avilov, Sergiy; Eimer, Stefan; Hein, Lutz; Pfanner, Nikolaus; Becker, Thomas; Akhtar, Asifa.

In: CELL, Vol. 167, No. 3, 20.10.2016, p. 722-738.e23.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Chatterjee, A, Seyfferth, J, Lucci, J, Gilsbach, R, Preissl, S, Böttinger, L, Mårtensson, CU, Panhale, A, Stehle, T, Kretz, O, Sahyoun, AH, Avilov, S, Eimer, S, Hein, L, Pfanner, N, Becker, T & Akhtar, A 2016, 'MOF Acetyl Transferase Regulates Transcription and Respiration in Mitochondria', CELL, vol. 167, no. 3, pp. 722-738.e23. https://doi.org/10.1016/j.cell.2016.09.052

APA

Chatterjee, A., Seyfferth, J., Lucci, J., Gilsbach, R., Preissl, S., Böttinger, L., Mårtensson, C. U., Panhale, A., Stehle, T., Kretz, O., Sahyoun, A. H., Avilov, S., Eimer, S., Hein, L., Pfanner, N., Becker, T., & Akhtar, A. (2016). MOF Acetyl Transferase Regulates Transcription and Respiration in Mitochondria. CELL, 167(3), 722-738.e23. https://doi.org/10.1016/j.cell.2016.09.052

Vancouver

Chatterjee A, Seyfferth J, Lucci J, Gilsbach R, Preissl S, Böttinger L et al. MOF Acetyl Transferase Regulates Transcription and Respiration in Mitochondria. CELL. 2016 Oct 20;167(3):722-738.e23. https://doi.org/10.1016/j.cell.2016.09.052

Bibtex

@article{8e2804f5478c4ccf87f37610f983aeb3,
title = "MOF Acetyl Transferase Regulates Transcription and Respiration in Mitochondria",
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.",
keywords = "Animals, Cardiomyopathy, Hypertrophic, Cell Respiration, DNA, Mitochondrial, Energy Metabolism, Epigenesis, Genetic, HeLa Cells, Heart Failure, Histone Acetyltransferases, Humans, Mice, Mice, Knockout, Mitochondria, Heart, Mitochondria, Muscle, Myocytes, Cardiac, Nuclear Proteins, Oxidative Phosphorylation, Transcription Factors, Transcription, Genetic, Journal Article, Research Support, Non-U.S. Gov't",
author = "Aindrila Chatterjee and Janine Seyfferth and Jacopo Lucci and Ralf Gilsbach and Sebastian Preissl and Lena B{\"o}ttinger and M{\aa}rtensson, {Christoph U} and Amol Panhale and Thomas Stehle and Oliver Kretz and Sahyoun, {Abdullah H} and Sergiy Avilov and Stefan Eimer and Lutz Hein and Nikolaus Pfanner and Thomas Becker and Asifa Akhtar",
note = "Copyright {\textcopyright} 2016 Elsevier Inc. All rights reserved.",
year = "2016",
month = oct,
day = "20",
doi = "10.1016/j.cell.2016.09.052",
language = "English",
volume = "167",
pages = "722--738.e23",
journal = "CELL",
issn = "0092-8674",
publisher = "Cell Press",
number = "3",

}

RIS

TY - JOUR

T1 - MOF Acetyl Transferase Regulates Transcription and Respiration in Mitochondria

AU - Chatterjee, Aindrila

AU - Seyfferth, Janine

AU - Lucci, Jacopo

AU - Gilsbach, Ralf

AU - Preissl, Sebastian

AU - Böttinger, Lena

AU - Mårtensson, Christoph U

AU - Panhale, Amol

AU - Stehle, Thomas

AU - Kretz, Oliver

AU - Sahyoun, Abdullah H

AU - Avilov, Sergiy

AU - Eimer, Stefan

AU - Hein, Lutz

AU - Pfanner, Nikolaus

AU - Becker, Thomas

AU - Akhtar, Asifa

N1 - Copyright © 2016 Elsevier Inc. All rights reserved.

PY - 2016/10/20

Y1 - 2016/10/20

N2 - 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.

AB - 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.

KW - Animals

KW - Cardiomyopathy, Hypertrophic

KW - Cell Respiration

KW - DNA, Mitochondrial

KW - Energy Metabolism

KW - Epigenesis, Genetic

KW - HeLa Cells

KW - Heart Failure

KW - Histone Acetyltransferases

KW - Humans

KW - Mice

KW - Mice, Knockout

KW - Mitochondria, Heart

KW - Mitochondria, Muscle

KW - Myocytes, Cardiac

KW - Nuclear Proteins

KW - Oxidative Phosphorylation

KW - Transcription Factors

KW - Transcription, Genetic

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1016/j.cell.2016.09.052

DO - 10.1016/j.cell.2016.09.052

M3 - SCORING: Journal article

C2 - 27768893

VL - 167

SP - 722-738.e23

JO - CELL

JF - CELL

SN - 0092-8674

IS - 3

ER -