Allostery is central to catalysis and regulation, yet how distal perturbations control enzyme activity remains unresolved. Here we elucidate how a distal allosteric hot spot regulates catalysis in dihydrofolate reductase, a benchmark enzyme exhibiting latent allostery. We combine enhanced conformational sampling, reactive free-energy calculations of the chemical step, and perturbation-induced nonequilibrium molecular dynamics with evolutionary analysis and experimental kinetics to obtain a comprehensive molecular description of conformational landscapes, catalytic activity, and allosteric communication. We show that a mutational perturbation at the hot spot redistributes the populations of two globally similar conformations with a subtle but critical structural difference that makes one catalytically competent and the other not. Nonequilibrium simulations further reveal that the transition between these two states proceeds through a stepwise sequence of local structural rearrangements rather than through concerted global motions or equilibrium fluctuations. Guided by this mechanism, we rationally engineer a compensatory second-site mutation that partially restores activity. These results provide a unified thermodynamic and kinetic view of allostery and establish a general, mechanistically guided framework for engineering allosteric regulation in enzymes.
No takes yet. Share an insight, caveat, or question.
Guénon et al. (2026) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: