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- W2114720004 abstract "ABSTRACT It has been reported that targeted disruption of ampD I or mrcA causes β-lactamase hyperproduction in Stenotrophomonas maltophilia . We show here that β-lactamase-hyperproducing laboratory selected mutants and clinical isolates can have wild-type ampD I and mrcA genes, implicating mutation of at least one additional gene in this phenotype. The involvement of mutations at multiple loci in the activation of β-lactamase production in S. maltophilia reveals that there are significant deviations from the enterobacterial paradigm of AmpR-mediated control of β-lactamase induction. We do show, however, that S. maltophilia ampD I can complement a mutation in Escherichia coli ampD . This suggests that an anhydromuropeptide degradation product of peptidoglycan is used to activate AmpR in S. maltophilia , as is also the case in enteric bacteria." @default.
- W2114720004 created "2016-06-24" @default.
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- W2114720004 date "2013-11-01" @default.
- W2114720004 modified "2023-10-16" @default.
- W2114720004 title "Involvement of Mutation in <i>ampD</i> I, <i>mrcA</i> , and at Least One Additional Gene in β-Lactamase Hyperproduction in Stenotrophomonas maltophilia" @default.
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- W2114720004 doi "https://doi.org/10.1128/aac.01446-13" @default.
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