Datasets

Title	OXPHOS deficiency activates global adaptation pathways to maintain mitochondrial membrane potential
Organism
Number of Samples	8
Release Date	2020/11/26 00:00
Sequencing Types
Protocol Details

Title
Authors	Liu S,Liu S,He B,Li L,Li L,Wang J,Cai T,Chen S,Jiang H
Journal	EMBO reports
Publication Date	2021 Apr 7
Abstract	Reduction of mitochondrial membrane potential (Δψ m ) is a hallmark of mitochondrial dysfunction. It activates adaptive responses in organisms from yeast to human to rewire metabolism, remove depolarized mitochondria, and degrade unimported precursor proteins. It remains unclear how cells maintain Δψ m , which is critical for maintaining iron-sulfur cluster (ISC) synthesis, an indispensable function of mitochondria. Here, we show that yeast oxidative phosphorylation mutants deficient in complex III, IV, V, and mtDNA, respectively, exhibit activated stress responses and progressive reduction of Δψ m . Extensive omics analyses of these mutants show that these mutants progressively activate adaptive responses, including transcriptional downregulation of ATP synthase inhibitor Inh1 and OXPHOS subunits, Puf3-mediated upregulation of import receptor Mia40 and global mitochondrial biogenesis, Snf1/AMPK-mediated upregulation of glycolysis and repression of ribosome biogenesis, and transcriptional upregulation of cytoplasmic chaperones. These adaptations disinhibit mitochondrial ATP hydrolysis, remodel mitochondrial proteome, and optimize ATP supply to mitochondria to convergently maintain Δψ m , ISC biosynthesis, and cell proliferation. © 2021 The Authors.
PMC	PMC8025004
PMID	33655635
DOI

Liu et al. 2020 (PRJNA680923)