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The first reported bla GMA-1 gene encoding gammaproteobacterial mobile class A β-lactamase (GMA-1) was identified in a recently defined mobile DNA element, a strand-biased circularizing integrative element (SE). Increased genomic data revealed the presence of bla GMA-1 in marine bacteria, including pathogenic species such as Vibrio parahaemolyticus and Photobacterium damselae . Herein, we address the substrate range of GMA-1 and how frequently bla GMA-1 was acquired by the chromosomes or plasmids via SEs using sequences in a publicly available database. An Escherichia coli strain carrying bla GMA-1 exhibited resistance to amoxicillin, piperacillin, and carbenicillin, but it remained susceptible to cephalosporins, monobactam, and carbapenems, indicating that GMA-1 belongs to functional group 2c, narrow-spectrum β-lactamases. bla GMA-1 -flanking sequence analysis for sequences in the RefSeq/GenBank database revealed a total of eight distinct SE-mediated bla GMA-1 acquisition events and six SE-independent bla GMA-1 acquisition events, including bla GMA-1 alone translocation, without involving a specific insertion sequence, or integron. Thus, this study shows that GMA-1 is specialized for penicillin degradation and is mainly disseminated by SEs; however, SE is not the only genetic mechanism transmitting bla GMA-1 . IMPORTANCE Despite increasing reports, class A β-lactamases of environmental bacteria remain very poorly characterized, with limited understanding of their transmission patterns. To address this knowledge gap, we focused on a recently designated GMA family β-lactamase gene, bla GMA-1 , found in marine bacterial genera such as Vibrio . This study shows that gammaproteobacterial mobile class A β-lactamase is specialized for penicillin degradation, and bla GMA-1 is frequently linked to strand-biased circularizing integrative elements (SEs) in sequences in the RefSeq/GenBank database. Evidence for the implication of SEs in β-lactamase environmental transmission provides insights for future surveillance studies of antimicrobial resistance genes in human clinical settings.
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Yano et al. (2023) studied this question.
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