ArticleCommunications chemistry2024
Mechanism of activation and autophosphorylation of a histidine kinase.
Article in Communications chemistry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Review
- Functional Characterization of the Histidine Kinase BaeS Reveals Critical Residues for BaeSR-Dependent Stress Signaling inMicroorganisms · 2026Article
- Integrated metabolomics and metagenomics uncover pathogenic mechanisms of Fusarium wilt and faba bean defense responses.NPJ science of food · 2026Article
- The regulatory role of histidine kinase in modulating nucleoside metabolites inFrontiers in microbiology · 2026Article
- The GHKL ATPase Family as a Paradigm for MutL Homolog Function in DNA Mismatch Repair.International journal of molecular sciences · 2025Review
- Molecular Characterization of the Group A Streptococcus Virulence-Regulatory System FasBCAX.Molecular microbiology · 2025Article
- Untangling the Complexity of Two-Component Signal Transduction in Bacteria.Microorganisms · 2025Review
- Two-Component System Sensor Kinase Inhibitors Target the ATP-Lid of PmrB to Disrupt Colistin Resistance inBiochemistry · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Histidine kinases (HK) are one of the main prokaryotic signaling systems. Two structurally conserved catalytic domains inside the HK enable autokinase, phosphotransfer, and phosphatase activities. Here, we focus on a detailed mechanistic understanding of the functional cycle of the WalK HK by a multi-scale simulation approach, consisting of classical as well as hybrid QM/MM molecular dynamics simulation. Strikingly, a conformational transition induced solely in DHp leads to the correct activated conformation in CA crucial for autophosphorylation. This finding explains how variable sensor domains induce the transition from inactive to active state. The subsequent autophosphorylation inside DHp proceeds via a penta-coordinated transition state to a protonated phosphohistidine intermediate. This intermediate is consequently deprotonated by a suitable nearby base. The reaction energetics are controlled by the final proton acceptor and presence of a magnesium cation. The slow rates of the process result from the high energy barrier of the conformational transition between inactive and active states. The phosphorylation step exhibits a lower barrier and down-the-hill energetics. Thus, our work suggests a detailed mechanistic model for HK autophosphorylation.
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Registered trials
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