Molecular mechanism of Arp2/3 complex activation by nucleation-promoting factors and an actin monomer
Arp (actin-related protein) 2/3 complex nucleates actin filament branches on the sides of preexisting actin filaments during cell and organelle movements. We used computer simulations of mammalian Arp2/3 complex to address fundamental questions about the mechanism. Metadynamics and umbrella free energy sampling simulations of the pathway revealed that a clash between the D-loop of Arp2 and Arp3 produces an energy barrier of 20 ± 6 kcal/mol between the inactive splayed and active short-pitch conformations of Arp2/3 complex. Atomistic molecular dynamics simulations showed that binding the CA motif of the nucleation-promoting factor Neuronal Wiskott-Aldrich Syndrome Protein (N-WASp) to inactive, splayed Arp2/3 complex shifts it toward the short-pitch active conformation and opens a binding site for an actin monomer on Arp3. Other simulations showed that this actin monomer stabilizes a transition state of Arp2/3 complex. These observations together with prior experimental work provide insights required to propose a physically grounded pathway for actin filament branch formation.
Authors
- Sahithya S. Iyer (ORCID: https://orcid.org/0009-0000-5591-5177)
- Jiangbo Wu (ORCID: https://orcid.org/0009-0002-7716-6079)
- Thomas D. Pollard (ORCID: https://orcid.org/0000-0002-1785-2969)
- Gregory A. Voth (ORCID: https://orcid.org/0000-0002-3267-6748)
Institutions
- Chicago Institute for Psychoanalysis (US)
- Yale University (US)
- University of Chicago (US)
Publication Details
- Journal
- Proceedings of the National Academy of Sciences
- Published
- 2025-03-06
- DOI
- https://doi.org/10.1073/pnas.2421467122
- Citations
- 2
- Primary Topic
- Cellular Mechanics and Interactions
- Type
- article
- Field-Weighted Citation Impact
- 2.30
Funders
- National Institutes of Health
- National Institute of General Medical Sciences