Time-resolved cryo-EM of G-protein activation by a GPCR.
Papasergi-Scott, M.M., Perez-Hernandez, G., Batebi, H., Gao, Y., Eskici, G., Seven, A.B., Panova, O., Hilger, D., Casiraghi, M., He, F., Maul, L., Gmeiner, P., Kobilka, B.K., Hildebrand, P.W., Skiniotis, G.(2024) Nature 629: 1182-1191
- PubMed: 38480881 
- DOI: https://doi.org/10.1038/s41586-024-07153-1
- Primary Citation of Related Structures:  
8GDZ, 8GE1, 8GE2, 8GE3, 8GE4, 8GE5, 8GE6, 8GE7, 8GE8, 8GE9, 8GEA, 8GEB, 8GEC, 8GED, 8GEE, 8GEF, 8GEG, 8GEH, 8GEI, 8GEJ, 8GFV, 8GFW, 8GFX, 8GFY, 8GFZ, 8GG0, 8GG1, 8GG2, 8GG3, 8GG4, 8GG5, 8GG6, 8GG7, 8GG8, 8GG9, 8GGA, 8GGB, 8GGC, 8GGE, 8GGF, 8GGI, 8GGJ, 8GGK, 8GGL, 8GGM, 8GGN, 8GGO, 8GGP, 8GGQ, 8GGR - PubMed Abstract: 
G-protein-coupled receptors (GPCRs) activate heterotrimeric G proteins by stimulating guanine nucleotide exchange in the G¦Á subunit 1 . To visualize this mechanism, we developed a time-resolved cryo-EM approach that examines the progression of ensembles of pre-steady-state intermediates of a GPCR-G-protein complex. By monitoring the transitions of the stimulatory G s protein in complex with the ¦Â 2 -adrenergic receptor at short sequential time points after GTP addition, we identified the conformational trajectory underlying G-protein activation and functional dissociation from the receptor. Twenty structures generated from sequential overlapping particle subsets along this trajectory, compared to control structures, provide a high-resolution description of the order of main events driving G-protein activation in response to GTP binding. Structural changes propagate from the nucleotide-binding pocket and extend through the GTPase domain, enacting alterations to G¦Á switch regions and the ¦Á5 helix that weaken the G-protein-receptor interface. Molecular dynamics simulations with late structures in the cryo-EM trajectory support that enhanced ordering of GTP on closure of the ¦Á-helical domain against the nucleotide-bound Ras-homology domain correlates with ¦Á5 helix destabilization and eventual dissociation of the G protein from the GPCR. These findings also highlight the potential of time-resolved cryo-EM as a tool for mechanistic dissection of GPCR signalling events.
Organizational Affiliation: 
Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA, USA.