bims-cytox1 Biomed News
on Cytochrome oxidase subunit 1
Issue of 2023–04–16
two papers selected by
Gavin McStay, Liverpool John Moores University
  1. Interaction of Terminal Oxidases with Amphipathic Molecules.
  2. Metabolic regulation of misfolded protein import into mitochondria.
  1. Int J Mol Sci. 2023 Mar 29. pii: 6428. [Epub ahead of print]24(7):
    Interaction of Terminal Oxidases with Amphipathic Molecules.
    Natalia V Azarkina, Vitaliy B Borisov, Ilya P Oleynikov, Roman V Sudakov, Tatiana V Vygodina.
      The review focuses on recent advances regarding the effects of natural and artificial amphipathic compounds on terminal oxidases. Terminal oxidases are fascinating biomolecular devices which couple the oxidation of respiratory substrates with generation of a proton motive force used by the cell for ATP production and other needs. The role of endogenous lipids in the enzyme structure and function is highlighted. The main regularities of the interaction between the most popular detergents and terminal oxidases of various types are described. A hypothesis about the physiological regulation of mitochondrial-type enzymes by lipid-soluble ligands is considered.
    Keywords:  amphipathic ligands; bile acid-binding site; cytochrome oxidase; detergents; molecular bioenergetics; regulation; terminal oxidases; tight bound lipids
    DOI:  https://doi.org/10.3390/ijms24076428
  2. bioRxiv. 2023 Mar 29. pii: 2023.03.29.534670. [Epub ahead of print]
    Metabolic regulation of misfolded protein import into mitochondria.
    Yuhao Wang, Linhao Ruan, Jin Zhu, Xi Zhang, Alexander Chih-Chieh Chang, Alexis Tomaszewski, Rong Li.
      Mitochondria are the cellular energy hub and central target of metabolic regulation. Mitochondria also facilitate proteostasis through pathways such as the 'mitochondria as guardian in cytosol' (MAGIC) whereby cytosolic misfolded proteins are imported into and degraded inside mitochondria. In this study, a genome-wide screen in yeast uncovered that Snf1, the yeast AMP-activated protein kinase (AMPK), inhibits the import of misfolded proteins into mitochondria while promoting mitochondrial biogenesis under glucose starvation. We show that this inhibition requires a downstream transcription factor regulating mitochondrial gene expression and is likely to be conferred through substrate competition and mitochondrial import channel selectivity. We further show that Snf1/AMPK activation protects mitochondrial fitness in yeast and human cells under stress induced by misfolded proteins such as those associated with neurodegenerative diseases.
    DOI:  https://doi.org/10.1101/2023.03.29.534670
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