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Reduction of Hypoiodous Acid by Shewanella oneidensis MR ‐1 Using Extracellular Electron Transfer Components

Jiani Zhang; Lingyu Hou; Sen Yan; Zhou Jiang; Yiran Dong; Liang Shi; Yongguang Jiang
Environmental Microbiology · Vol. 28, Issue 3 · 2026

Abstract

Hypoiodous acid (HIO) represents a pivotal iodine species in global iodine cycling, yet microbial contributions to its transformation have remained poorly characterised. Here, we demonstrate that the metal‐reducing bacterium Shewanella oneidensis MR‐1 actively drive HIO reduction to iodide. Notably, genetic disruption of extracellular electron transfer components impaired HIO reduction activity in S. oneidensis MR‐1. Specifically, Δ mtrCAB reduced 49.7% less HIO than the wild type within 10 min, while Δ dmsEFAB exhibited a slight impairment in HIO reduction. The mutants lacking outer‐membrane c ‐type cytochromes (MtrC and OmcA) also showed substantially lower reduction efficiencies (29.6%–54.0%) than wild type. Although flavin secretion was not essential for HIO reduction in S. oneidensis MR‐1, reduced riboflavin chemically reacted with HIO to generate iodide. Importantly, both the mtrC / omcA deletions and exogenous HIO addition inhibited iodate reduction, suggesting HIO reduction serves as a detoxification mechanism. In contrast, electron shuttles dose‐dependently enhanced iodate reduction. Collectively, these results demonstrate that Shewanella ‐mediated HIO reduction constitutes a rapid detoxifying pathway for HIO, with the MtrCAB‐OmcA transmembrane electron conduit acting as the primary mediator. However, the DmsEFAB pathway and endogenous electron shuttles showed limited contributions.

Bibliographic Information

JournalEnvironmental Microbiology
PublisherWiley
Publication Date2026-03-01
Publication Year2026
Volume28
Issue3
Document TypeJournal Article
Print ISSN1462-2912
eISSN1462-2920
DOI10.1111/1462-2920.70281
SubjectMicrobial Ecology

Access Information

NARA Access Coverage1999-01-01~Current
Journal Homepagehttps://onlinelibrary.wiley.com/loi/14622920
Publisher PageOpen Publisher Page
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