Manipulating mtDNA in vivo reprograms metabolism via novel response mechanisms.

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ID: 84895
2019
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Abstract
Mitochondria have been increasingly recognized as a central regulatory nexus for multiple metabolic pathways, in addition to ATP production via oxidative phosphorylation (OXPHOS). Here we show that inducing mitochondrial DNA (mtDNA) stress in Drosophila using a mitochondrially-targeted Type I restriction endonuclease (mtEcoBI) results in unexpected metabolic reprogramming in adult flies, distinct from effects on OXPHOS. Carbohydrate utilization was repressed, with catabolism shifted towards lipid oxidation, accompanied by elevated serine synthesis. Cleavage and translocation, the two modes of mtEcoBI action, repressed carbohydrate rmetabolism via two different mechanisms. DNA cleavage activity induced a type II diabetes-like phenotype involving deactivation of Akt kinase and inhibition of pyruvate dehydrogenase, whilst translocation decreased post-translational protein acetylation by cytonuclear depletion of acetyl-CoA (AcCoA). The associated decrease in the concentrations of ketogenic amino acids also produced downstream effects on physiology and behavior, attributable to decreased neurotransmitter levels. We thus provide evidence for novel signaling pathways connecting mtDNA to metabolism, distinct from its role in supporting OXPHOS.
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bahhir2019manipulatingplos Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Bahhir, Diana;Yalgin, Cagri;Ots, Liina;Järvinen, Sampsa;George, Jack;Naudí, Alba;Krama, Tatjana;Krams, Indrikis;Tamm, Mairi;Andjelković, Ana;Dufour, Eric;González de Cózar, Jose M;Gerards, Mike;Parhiala, Mikael;Pamplona, Reinald;Jacobs, Howard T;Jõers, Priit;
Journal PLoS genetics
Year 2019
DOI
10.1371/journal.pgen.1008410
URL
Keywords
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