Document Detail


An engineered disulfide bond between residues 69 and 238 in extended-spectrum beta-lactamase Toho-1 reduces its activity toward third-generation cephalosporins.
MedLine Citation:
PMID:  15595829     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Previous crystallographic structural analysis of extended-spectrum beta-lactamase Toho-1 predicted that the high flexibility of beta-strand B3, the region that contains a conserved KTG motif and forms one wall of the substrate-binding site, could be one of the key features contributing to Toho-1 activity toward third-generation cephalosporins. To investigate whether this possible flexibility really affects the substrate profile of this enzyme, two Toho-1 mutants have been produced, G238C and G238C/G239in, in which the glycine residue at position 238 was replaced with a cysteine and an additional glycine residue was inserted. Our intent was to introduce a disulfide bond between the cysteine residues at positions 69 and 238, and thus to lock the position of beta-strand B3. The results of 5,5'-dithiobis(2-nitrobenzoic acid) (DTNB) titration indicated formation of a new disulfide bridge in the G238C mutant, although disulfide bond formation was not confirmed in the G238C/G239in mutant. Kinetic analysis showed that the activity of the G238C mutant decreased drastically against third-generation cephalosporins, while its catalytic efficiency against penicillins and first-generation cephalosporins was almost identical to that of the wild-type enzyme. This result was consistent with the prediction that flexibility in beta-strand B3 was critical for activity against third-generation cephalosporins in Toho-1. Furthermore, we have determined the crystal structure of the G238C mutant enzyme to analyze the structural changes in detail. The structural model clearly shows the introduction of a new disulfide bridge and that there is no appreciable difference between the overall structures of the wild-type enzyme and the G238C mutant, although the introduced disulfide bond slightly influenced the positions of Ser237 on beta-strand B3 and Asn170 on the Omega loop. The results of our kinetic and structural analyses suggest that the flexibility of beta-strand B3, as well as the positions of Ser237 and the Omega loop, is critical for the substrate specificity expansion of Toho-1.
Authors:
Akiko Shimizu-Ibuka; Hiroshi Matsuzawa; Hiroshi Sakai
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Biochemistry     Volume:  43     ISSN:  0006-2960     ISO Abbreviation:  Biochemistry     Publication Date:  2004 Dec 
Date Detail:
Created Date:  2004-12-14     Completed Date:  2005-02-07     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0370623     Medline TA:  Biochemistry     Country:  United States    
Other Details:
Languages:  eng     Pagination:  15737-45     Citation Subset:  IM    
Affiliation:
Department of Food and Nutritional Sciences, University of Shizuoka, 52-1 Yada, Shizuoka 422-8526, Japan. aibuka@mail.ecc.u-tokyo.ac.jp
Data Bank Information
Bank Name/Acc. No.:
PDB/1WE4
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MeSH Terms
Descriptor/Qualifier:
Amino Acid Sequence
Binding Sites / genetics
Cephalosporins / chemistry,  metabolism*
Crystallography, X-Ray
Disulfides / chemistry*
Dithionitrobenzoic Acid / chemistry
Escherichia coli Proteins / chemistry*,  genetics,  metabolism*
Molecular Sequence Data
Point Mutation / genetics
Protein Engineering
Protein Structure, Secondary
Sequence Alignment
Substrate Specificity
beta-Lactamases / chemistry*,  genetics,  metabolism*
Chemical
Reg. No./Substance:
0/Cephalosporins; 0/Disulfides; 0/Escherichia coli Proteins; 69-78-3/Dithionitrobenzoic Acid; EC 3.5.2.6/beta-Lactamases; EC 3.5.2.6/beta-lactamase Toho-1, E coli

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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