23UL image
Deposition Date 2026-02-18
Release Date 2026-10-21
Last Version Date 2026-10-21
Entry Detail
PDB ID:
23UL
Keywords:
Title:
Crystal Structure of Aquifex aeolicus GyrB ATPase domain complexed with AMPPNP
Biological Source:
Source Organism(s):
Expression System(s):
Method Details:
Experimental Method:
Resolution:
1.65 Å
R-Value Free:
0.21
R-Value Work:
0.19
R-Value Observed:
0.19
Space Group:
P 2 21 21
Macromolecular Entities
Polymer Type:polypeptide(L)
Molecule:Type 2 topoisomerase subunit
Gene (Uniprot):gyrB
Chain IDs:A, B
Chain Length:397
Number of Molecules:2
Biological Source:Aquifex aeolicus VF5
Primary Citation
Two Glu/Asp residues cooperatively mediate an early step of ATP hydrolysis in GHKL ATPases MutL and GyrB.
Elife 15 ? ? (2026)
PMID: 42788712 DOI: 10.7554/eLife.111443

Abstact

GHKL ATPases share a unique Bergerat ATP-binding fold and regulate diverse biological processes through ATP-dependent conformational changes. An early step of ATP hydrolysis in this family has been attributed to a single highly conserved glutamate residue proposed to function as the general base. However, mutations of this residue impair both the ATPase activity and ATP binding, complicating interpretation of its catalytic role. Re-examination of the high-resolution crystal structures revealed a second conserved acidic residue positioned within a hydrogen-bonding distance from the nucleophilic water molecule. Using Aquifex aeolicus MutL and GyrB as model enzymes, we combined systematic mutagenesis, ATPase and ATP-binding assays, and X-ray crystallography to dissect the roles of these residues. We show that alignment of the nucleophilic water can be maintained as long as the conserved glutamate retains hydrogen-bonding capability, whereas efficient ATP hydrolysis requires proton-accepting capacity at least in one of the two acidic residues. These results indicate that the conserved glutamate primarily governs positioning of the nucleophilic water, while activation of this water for catalysis is achieved through cooperative general base function of the two acidic residues. Extending this framework to human MutL homologs, PMS2 and MLH1, we showed that clinically reported variants of uncertain significance in these DNA mismatch repair proteins substantially reduced the ATPase activity, indicating functional impairment. Together, our findings refine the catalytic mechanism of GHKL ATPases and provide a structural and functional framework for interpreting disease-associated variants in GHKL ATPases. Phylogenetic and ancestral state analysis further indicated that the second acidic residue was likely to be present in the common ancestor of major GHKL ATPase lineages but was later modified in a branch, including Hsp90, suggesting evolutionary remodeling of the catalytic mechanism in the branch.

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