6D9T

BshA from Staphylococcus aureus complexed with UDP


Experimental Data Snapshot

  • Method: X-RAY DIFFRACTION
  • Resolution: 2.00 Å
  • R-Value Free: 0.188 
  • R-Value Work: 0.168 
  • R-Value Observed: 0.169 

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Ligand Structure Quality Assessment 


This is version 1.3 of the entry. See complete history


Literature

A structural and functional analysis of the glycosyltransferase BshA from Staphylococcus aureus: Insights into the reaction mechanism and regulation of bacillithiol production.

Royer, C.J.Cook, P.D.

(2019) Protein Sci 28: 1083-1094

  • DOI: https://doi.org/10.1002/pro.3617
  • Primary Citation of Related Structures:  
    6D9T, 6N1X

  • PubMed Abstract: 

    Bacillithiol is a glucosamine-derived antioxidant found in several pathogenic Gram-positive bacteria. The compound is involved in maintaining the appropriate redox state within the cell as well as detoxifying foreign agents like the antibiotic fosfomycin. Bacillithiol is produced via the action of three enzymes, including BshA, a retaining GT-B glycosyltransferase that utilizes UDP-N-acetylglucosamine and l-malate to produce N-acetylglucosaminyl-malate. Recent studies suggest that retaining GT-B glycosyltransferases like BshA utilize a substrate-assisted mechanism that goes through an S N i-like transition state. In a previous study, we relied on X-ray crystallography as well as computational simulations to hypothesize the manner in which substrates would bind the enzyme, but several questions about substrate binding and the role of one of the amino acid residues persisted. Another study demonstrated that BshA might be subject to feedback inhibition by bacillithiol, but this phenomenon was not analyzed further to determine the exact mechanism of inhibition. Here we present X-ray crystallographic structures and steady-state kinetics results that help elucidate both of these issues. Our ligand-bound crystal structures demonstrate that the active site provides an appropriate steric and geometric arrangement of ligands to facilitate the substrate-assisted mechanism. Finally, we show that bacillithiol is competitive for UDP-N-acetylglucosamine with a K i value near 120-130 μM and likely binds within the BshA active site, suggesting that bacillithiol modulates BshA activity via feedback inhibition. The work presented here furthers our understanding of bacillithiol metabolism and can aid in the development of inhibitors to counteract resistance to antibiotics such as fosfomycin.


  • Organizational Affiliation

    Department of Chemistry, Grand Valley State University, Allendale, Michigan.


Macromolecules
Find similar proteins by:  (by identity cutoff)  |  3D Structure
Entity ID: 1
MoleculeChains Sequence LengthOrganismDetailsImage
Glycosyl transferase400Staphylococcus aureusMutation(s): 0 
Gene Names: pimB_2BTN44_05260EP54_02400EQ90_10145ERS365775_02315
EC: 2.4.1.57
UniProt
Find proteins for A0A068A5A2 (Staphylococcus aureus)
Explore A0A068A5A2 
Go to UniProtKB:  A0A068A5A2
Entity Groups  
Sequence Clusters30% Identity50% Identity70% Identity90% Identity95% Identity100% Identity
UniProt GroupA0A068A5A2
Sequence Annotations
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  • Reference Sequence
Experimental Data & Validation

Experimental Data

  • Method: X-RAY DIFFRACTION
  • Resolution: 2.00 Å
  • R-Value Free: 0.188 
  • R-Value Work: 0.168 
  • R-Value Observed: 0.169 
  • Space Group: P 2 3
Unit Cell:
Length ( Å )Angle ( ˚ )
a = 135.38α = 90
b = 135.38β = 90
c = 135.38γ = 90
Software Package:
Software NamePurpose
Aimlessdata scaling
PHENIXrefinement
PDB_EXTRACTdata extraction
XDSdata reduction
PHASERphasing

Structure Validation

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Ligand Structure Quality Assessment 


Entry History & Funding Information

Deposition Data


Funding OrganizationLocationGrant Number
National Institutes of Health/National Institute of General Medical Sciences (NIH/NIGMS)United States1R15GM117488

Revision History  (Full details and data files)

  • Version 1.0: 2019-05-08
    Type: Initial release
  • Version 1.1: 2019-10-30
    Changes: Data collection, Database references
  • Version 1.2: 2020-01-01
    Changes: Author supporting evidence
  • Version 1.3: 2023-10-04
    Changes: Data collection, Database references, Refinement description