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Structure-function analysis of exotoxin A proteins with mutations at histidine 426

M J Wick1, J M Cook, B H Iglewski

  • 1Department of Microbiology and Immunology, University of Rochester School of Medicine and Dentistry, New York 14642.

Insights

Histidine-426 in Pseudomonas aeruginosa exotoxin A is crucial for its ADP-ribosyltransferase and NAD-glycohydrolase activity. Substituting this residue significantly reduces enzymatic function, indicating a key structural role in the catalytic site.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Microbiology

Background:

  • Pseudomonas aeruginosa exotoxin A is a potent toxin.
  • Previous studies indicated that substituting Tyrosine for Histidine-426 reduces ADP-ribosyltransferase activity.

Purpose of the Study:

  • To investigate the precise role of Histidine-426 in the enzymatic activity of Pseudomonas aeruginosa exotoxin A.
  • To determine if Histidine-426 has a catalytic function or a structural role in the enzyme's active site.

Main Methods:

  • Oligonucleotide-directed mutagenesis was used to create mutant exotoxin A proteins with substitutions at position 426 (Ala, Glu, Gly, Lys, Pro).
  • ADP-ribosyltransferase activity was measured using 34,000-Da carboxy-terminal exotoxin A peptides (H426n peptides).
  • NAD-glycohydrolase activity was measured for full-size wild-type and mutant exotoxin A proteins (Ala-426, Tyr-426).

Main Results:

  • Mutant H426n peptides showed ADP-ribosyltransferase activity ranging from 0.002% to 28% of wild-type levels.
  • Exotoxin A mutants with Ala-426 or Tyr-426 exhibited less than 1% of wild-type NAD-glycohydrolase activity.
  • Wild-type and mutant full-size proteins displayed conformational differences, evidenced by enzymatic activation and tryptic digestion patterns.

Conclusions:

  • Histidine-426 is essential for the full expression of Pseudomonas aeruginosa exotoxin A's ADP-ribosyltransferase activity.
  • Histidine-426 appears to play a critical structural role in domain III, orienting active-site residues within the catalytic cleft.
  • The findings suggest His-426 is vital for maintaining the correct molecular architecture of the enzyme's active site.

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