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<p>Poplar bacterial canker, caused by <i>Lonsdalea populi</i>, seriously threatens the health of poplar plantations. The two-component system is one of the most important signal transduction pathways in bacteria, playing a crucial role in numerical traits including growth, stress tolerance, and pathogenicity; however, their functions in <i>L. populi</i> remain poorly understood. Here, we identified a two-component system (RstB/RstA) in <i>L. populi</i>. The deletion of either <i>rstB</i> or <i>rstA</i> led to a decrease in <i>L. populi</i> virulence, biofilm formation, and tolerance to H<sub>2</sub>O<sub>2</sub> and iron stresses. Based on transcriptomic data of the <i>rstB</i> or <i>rstA</i> mutants, an electrophoretic mobility shift assay confirmed that RstA directly binds to the promoter of <i>lpfetA</i>. Given that <i>lpfetA</i>, <i>lpfetB</i>, and <i>lpfetC</i> are co-transcribed as an operon, these results suggested that RstA likely regulates the <i>lpfetABC</i> operon. The overexpression of either <i>lpfetA</i>, <i>lpfetB</i>, or <i>lpfetC</i> almost abolished bacterial virulence, while resulted in decreased biofilm formation and tolerance to H<sub>2</sub>O<sub>2</sub>. These findings demonstrated that RstA modulates <i>L. populi</i> virulence, at least in part, by regulating the <i>lpfet</i> operon. Overall, our work indicated that RstB/RstA plays an important role in bacterial virulence and stress tolerance.</p>

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The two-component system RstB/RstA regulates virulence through the Fe3+-siderophore transport operon lpfetABC in the poplar canker bacterium Lonsdalea populi

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  • 发表日期：

    2025年12月2日

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  • Sha Zeng,
  • Ruirui Yang,
  • Zexu Ming,
  • Aining Li

摘要

Poplar bacterial canker, caused by Lonsdalea populi, seriously threatens the health of poplar plantations. The two-component system is one of the most important signal transduction pathways in bacteria, playing a crucial role in numerical traits including growth, stress tolerance, and pathogenicity; however, their functions in L. populi remain poorly understood. Here, we identified a two-component system (RstB/RstA) in L. populi. The deletion of either rstB or rstA led to a decrease in L. populi virulence, biofilm formation, and tolerance to H2O2 and iron stresses. Based on transcriptomic data of the rstB or rstA mutants, an electrophoretic mobility shift assay confirmed that RstA directly binds to the promoter of lpfetA. Given that lpfetA, lpfetB, and lpfetC are co-transcribed as an operon, these results suggested that RstA likely regulates the lpfetABC operon. The overexpression of either lpfetA, lpfetB, or lpfetC almost abolished bacterial virulence, while resulted in decreased biofilm formation and tolerance to H2O2. These findings demonstrated that RstA modulates L. populi virulence, at least in part, by regulating the lpfet operon. Overall, our work indicated that RstB/RstA plays an important role in bacterial virulence and stress tolerance.