Proton motive function of the terminal antiporter-like subunit in respiratory complex I

Biochim Biophys Acta Bioenerg. 2020 Jul 1;1861(7):148185. doi: 10.1016/j.bbabio.2020.148185. Epub 2020 Mar 19.

Abstract

In the aerobic respiratory chains of many organisms, complex I functions as the first electron input. By reducing ubiquinone (Q) to ubiquinol, it catalyzes the translocation of protons across the membrane as far as ~200 Å from the site of redox reactions. Despite significant amount of structural and biochemical data, the details of redox coupled proton pumping in complex I are poorly understood. In particular, the proton transfer pathways are extremely difficult to characterize with the current structural and biochemical techniques. Here, we applied multiscale computational approaches to identify the proton transfer paths in the terminal antiporter-like subunit of complex I. Data from combined classical and quantum chemical simulations reveal for the first time structural elements that are exclusive to the subunit, and enables the enzyme to achieve coupling between the spatially separated Q redox reactions and proton pumping. By studying long time scale protonation and hydration dependent conformational dynamics of key amino acid residues, we provide novel insights into the proton pumping mechanism of complex I.

Keywords: Cell respiration; Mitochondria; Proton transfer; Redox reactions.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Sequence
  • Antiporters / chemistry
  • Antiporters / metabolism*
  • Electron Transport Complex I / metabolism*
  • Models, Molecular
  • Protein Conformation
  • Protein Subunits / chemistry
  • Protein Subunits / metabolism*
  • Proton-Motive Force / physiology*
  • Protons
  • Salts / chemistry
  • Thermus thermophilus / metabolism
  • Water / chemistry

Substances

  • Antiporters
  • Protein Subunits
  • Protons
  • Salts
  • Water
  • Electron Transport Complex I