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<p>The transition metal zinc is an essential trace element for life but becomes toxic at high concentrations. In the opportunistic pathogen <i>Chromobacterium violaceum</i>, zinc acquisition is crucial for virulence, yet how this bacterium copes with zinc toxicity remains unknown. In this work, we demonstrate that <i>C. violaceum</i> senses and responds to excess zinc by activating the <i>zntA</i> gene, which encodes a P<sub>1B-2</sub>-type ATPase, via the transcriptional regulator ZntR. Phenotypic analyses by growth curves, disk diffusion, and CFU assays revealed that both Δ<i>zntA</i> or Δ<i>zntR</i> mutant strains exhibited increased sensitivity to zinc and cadmium. The Δ<i>zntA</i> mutant showed increased zinc and cadmium accumulation, suggesting that ZntA functions as an efflux pump. The expression of <i>zntA</i> increased in the presence of zinc and cadmium in the wild-type strain, but not in the Δ<i>zntR</i> mutant strain, indicating that ZntR activates <i>zntA</i> under conditions of zinc or cadmium excess. The role of ZntA in vivo was analyzed using the social amoeba <i>Dictyostelium discoideum</i> as a host cell. Plaque assays indicated that the <i>C. violaceum</i> Δ<i>zntA</i> mutant strain was more susceptible than the <i>C. violaceum</i> wild-type strain to clearance by <i>D. discoideum</i> knockout strains with altered intracellular zinc allocation. Overall, our data reveal that the genes <i>zntA</i> and <i>zntR</i> encoding a P<sub>1B-2</sub>-type ATPase and its transcriptional activator are key determinants of zinc and cadmium resistance in <i>C. violaceum</i>, ensuring bacterial survival under zinc-stress conditions encountered in the environment and the host.</p>

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The genes zntA and zntR encoding a P-type ATPase and its activator confer zinc and cadmium resistance in Chromobacterium violaceum

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  • 发表日期：

    2026年5月22日

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  • Carolina Panosso Schuindt,
  • Bianca Bontempi Batista,
  • Lucas Cesetti,
  • Sergio Pereira Lima Neto,
  • Thierry Soldati,
  • José Freire da Silva Neto

摘要

The transition metal zinc is an essential trace element for life but becomes toxic at high concentrations. In the opportunistic pathogen Chromobacterium violaceum, zinc acquisition is crucial for virulence, yet how this bacterium copes with zinc toxicity remains unknown. In this work, we demonstrate that C. violaceum senses and responds to excess zinc by activating the zntA gene, which encodes a P1B-2-type ATPase, via the transcriptional regulator ZntR. Phenotypic analyses by growth curves, disk diffusion, and CFU assays revealed that both ΔzntA or ΔzntR mutant strains exhibited increased sensitivity to zinc and cadmium. The ΔzntA mutant showed increased zinc and cadmium accumulation, suggesting that ZntA functions as an efflux pump. The expression of zntA increased in the presence of zinc and cadmium in the wild-type strain, but not in the ΔzntR mutant strain, indicating that ZntR activates zntA under conditions of zinc or cadmium excess. The role of ZntA in vivo was analyzed using the social amoeba Dictyostelium discoideum as a host cell. Plaque assays indicated that the C. violaceum ΔzntA mutant strain was more susceptible than the C. violaceum wild-type strain to clearance by D. discoideum knockout strains with altered intracellular zinc allocation. Overall, our data reveal that the genes zntA and zntR encoding a P1B-2-type ATPase and its transcriptional activator are key determinants of zinc and cadmium resistance in C. violaceum, ensuring bacterial survival under zinc-stress conditions encountered in the environment and the host.