Ca2+ binding induced sequential allosteric activation of sortase A: An example for ion-triggered conformational selection.
Ilke UgurMartin SchatteAntoine MarionManuel GlaserMara Boenitz-DulatIris AntesPublished in: PloS one (2018)
The allosteric activation of the intrinsically disordered enzyme Staphylococcus aureus sortase A is initiated via binding of a Ca2+ ion. Although Ca2+ binding was shown to initiate structural changes inducing disorder-to-order transitions, the details of the allosteric activation mechanism remain elusive. We performed long-term molecular dynamics simulations of sortase A without (3 simulations of 1.6 μs) and with bound Ca2+ (simulations of 1.6 μs, 1.8 μs, and 2.5 μs). Our results show that Ca2+ binding causes not only ordering of the disordered β6/β7 loop of the protein, but also modulates hinge motions in the dynamic β7/β8 loop, which is important for the catalytic activity of the enzyme. Cation binding triggers signal transmission from the Ca2+ binding site to the dynamic β7/β8 loop via the repetitive folding/unfolding of short helical stretches of the disordered β6/β7 loop. These correlated structural rearrangements lead to several distinct conformational states of the binding groove, which show optimal binding features for the sorting signal motif and feature binding energies up to 20 kcal/mol more favorable than observed for the sortase A without Ca2+. The presented results indicate a highly correlated, conformational selection-based activation mechanism of the enzyme triggered by cation binding. They also demonstrate the importance of the dynamics of intrinsically disordered regions for allosteric regulation.
Keyphrases
- molecular dynamics simulations
- staphylococcus aureus
- dna binding
- small molecule
- binding protein
- molecular dynamics
- transcription factor
- single molecule
- protein kinase
- molecular docking
- machine learning
- cystic fibrosis
- oxidative stress
- escherichia coli
- drug induced
- density functional theory
- neural network
- candida albicans
- methicillin resistant staphylococcus aureus