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Acinetobacter baumannii ATCC 17978 encodes a microcin system with antimicrobial properties for contact-independent competition
Journal article   Open access   Peer reviewed

Acinetobacter baumannii ATCC 17978 encodes a microcin system with antimicrobial properties for contact-independent competition

Fabiana Bisaro, Howard A Shuman, Mario F Feldman, Michael J Gebhardt and Stefan Pukatzki
Microbiology (Society for General Microbiology), Vol.169(6), 001346
06/01/2023
DOI: 10.1099/mic.0.001346
PMCID: PMC10333792
PMID: 37289493
url
https://doi.org/10.1099/mic.0.001346View
Published (Version of record) Open Access

Abstract

Acinetobacter baumannii is a multidrug-resistant opportunistic pathogen that persists in the hospital environment and causes various clinical infections, primarily affecting immunocompromised patients. A. baumannii has evolved a wide range of mechanisms to compete with neighbouring bacteria. One such competition strategy depends on small secreted peptides called microcins, which exert antimicrobial effects in a contact-independent manner. Here, we report that A. baumannii ATCC 17978 (AB17978) encodes the class II microcin 17 978 (Mcc17978) with antimicrobial activity against closely related Acinetobacter, and surprisingly, also Escherichia coli strains. We identified the genetic locus encoding the Mcc17978 system in AB17978. Using classical bacterial genetic approaches, we determined that the molecular receptor of Mcc17978 in E. coli is the iron-catecholate transporter Fiu, and in Acinetobacter is Fiu’s homolog, PiuA. In bacteria, the Ferric uptake regulator (Fur) positively regulates siderophore systems and microcin systems under iron-deprived environments. We found that the Mcc17978 system is upregulated under low-iron conditions commonly found in the host environment and identified a putative Fur binding site upstream of the mcc17978 gene. When we tested the antimicrobial activity of Mcc17978 under different levels of iron availability, we observed that low iron levels not only triggered transcriptional induction of the microcin, but also led to enhanced microcin activity. Taken together, our findings suggest that A. baumannii may utilize microcins to compete with other microbes for resources during infection.
Iron UIOWA OA Agreement Acinetobacter baumannii Fiu Iron uptake receptor Microcin PiuA

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