# Mechanisms of Arsenic Interaction in Bacillus subtilis and Related Species with Biotechnological Potential

**Authors:** Luz I. Valenzuela-García, María Teresa Alarcón-Herrera, Elizabeth Cisneros-Lozano, Mario Pedraza-Reyes, Víctor M. Ayala-García

PMC · DOI: 10.3390/ijms262110277 · International Journal of Molecular Sciences · 2025-10-22

## TL;DR

This paper reviews how Bacillus subtilis and related bacteria resist arsenic toxicity through various molecular mechanisms, with potential applications in bioremediation.

## Contribution

The paper provides a detailed analysis of arsenic resistance mechanisms in Bacillus species, focusing on the ars and ase operons and their biotechnological implications.

## Key findings

- Bacillus subtilis uses biosorption, redox transformation, and efflux pumps to resist arsenic.
- The ars operon includes genes like ArsC, ArsB, and ArsR, which are co-regulated in response to arsenic.
- Environmental Bacillus species show evolutionary adaptations and potential for bioremediation.

## Abstract

Arsenic (As) toxicity drives the evolution of resistance mechanisms in environmental microorganisms. Bacteria of the Bacillus genus are frequently identified in isolates from arsenic-contaminated sites, highlighting the importance of understanding the molecular mechanisms related to this bacterial genus. Bacillus subtilis, a soil microorganism and Gram-positive model paradigm, employs multiple strategies to counteract As toxicity, including biosorption, redox transformation, active efflux, and inducible genetic regulation. This review provides a comprehensive analysis of the physiological and molecular mechanisms involved in arsenic response in B. subtilis and related species, focusing on the ars and ase operons. The ars operon, located within the mobile SKIN element, encodes a reductase (ArsC), an Acr3-type efflux pump (ArsB), a carbon–arsenic lyase (ArsI/YqcK), and a transcriptional repressor (ArsR), all co-regulated in response to arsenic. In turn, the ase operon contributes to resistance via an ArsB-type efflux system (AseA) and its own regulatory protein (AseR) but lacks an arsenate reductase. Additionally, genes such as aioAB, arrAB, and arsD are discussed, along with evidence for extracellular detoxification and cell surface immobilization of As. Studies on environmental Bacillus species are examined, pointing out the evolutionary implications of As resistance and the biotechnological potential for remediation of contaminated sites.

## Linked entities

- **Genes:** STS (steroid sulfatase) [NCBI Gene 412], ARSB (arylsulfatase B) [NCBI Gene 411], arsR (ArsR family transcriptional regulator) [NCBI Gene 878629], aseR (transcriptional regulator (metals sensing ArsR-SmtB repressors family)) [NCBI Gene 938089], ARSD (arylsulfatase D) [NCBI Gene 414]
- **Chemicals:** arsenic (PubChem CID 5359596)
- **Species:** Bacillus subtilis (taxon 1423), Bacillus (taxon 1386)

## Full-text entities

- **Diseases:** toxicity (MESH:D064420)
- **Chemicals:** Arsenic (MESH:D001151)
- **Species:** Bacillus subtilis (species) [taxon 1423], Bacillus (genus) [taxon 55087]

## Full text

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## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12607644/full.md

## References

178 references — full list in the complete paper: https://tomesphere.com/paper/PMC12607644/full.md

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Source: https://tomesphere.com/paper/PMC12607644