Gαi1 inhibition mechanism of ATP-bound adenylyl cyclase type 5

PLoS One. 2021 Jan 25;16(1):e0245197. doi: 10.1371/journal.pone.0245197. eCollection 2021.

Abstract

Conversion of adenosine triphosphate (ATP) to the second messenger cyclic adenosine monophosphate (cAMP) is an essential reaction mechanism that takes place in eukaryotes, triggering a variety of signal transduction pathways. ATP conversion is catalyzed by the enzyme adenylyl cyclase (AC), which can be regulated by binding inhibitory, Gαi, and stimulatory, Gαs subunits. In the past twenty years, several crystal structures of AC in isolated form and complexed to Gαs subunits have been resolved. Nevertheless, the molecular basis of the inhibition mechanism of AC, induced by Gαi, is still far from being fully understood. Here, classical molecular dynamics simulations of the isolated holo AC protein type 5 and the holo binary complex AC5:Gαi have been analyzed to investigate the conformational impact of Gαi association on ATP-bound AC5. The results show that Gαi appears to inhibit the activity of AC5 by preventing the formation of a reactive ATP conformation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenylyl Cyclases / chemistry*
  • Cyclic AMP / chemistry*
  • GTP-Binding Protein alpha Subunits, Gi-Go / chemistry*
  • Humans
  • Molecular Dynamics Simulation*
  • Multiprotein Complexes / chemistry*
  • Protein Structure, Quaternary

Substances

  • Multiprotein Complexes
  • Cyclic AMP
  • GNAI1 protein, human
  • GTP-Binding Protein alpha Subunits, Gi-Go
  • Adenylyl Cyclases
  • adenylyl cyclase type V

Grants and funding

This work was supported by the Swiss National Science Foundation and computer time on the CSCS Piz Daint cluster. This project/research has received funding from the European Union’s Horizon 2020 Framework Programme for Research and Innovation under Specific Grant Agreement 720270 (Human Brain Project SGA1).