<p>The cultivation of plums is significantly endangered by bacterial shot-hole disease, which is caused by <i>Pantoea agglomerans</i>. This study evaluated the antibacterial efficacy of tetramycin against <i>P. agglomerans</i> in comparison with six conventional antibiotics. <i>In vitro</i> assays revealed that 0.3% tetramycin aqueous solutions (AS) exhibited potent inhibitory activity, with a half-maximal effective concentration (EC<sub>50</sub>) of 1.71&#xa0;μg/mL. To investigate the mechanistic basis of this activity, alterations in colony morphology, cell membrane permeability, biofilm formation, and energy metabolism were analyzed in tetramycin-treated <i>P. agglomerans</i>. Tetramycin exposure induced significant leakage of electrolytes and macromolecular substances, indicating severe disruption of cell membrane integrity. Concurrently, biofilm formation was markedly suppressed, with an inhibition rate of 51% at EC<sub>75</sub>. Furthermore, tetramycin altered bacterial metabolic activity, as evidenced by elevated pyruvate accumulation, reduced malate dehydrogenase activity, and decreased ATP levels, suggesting interference with energy metabolism pathways. In conclusion, tetramycin effectively inhibited <i>P. agglomerans</i> growth by disrupting cell membrane stability, suppressing biofilm formation, and impairing energy metabolism. These findings provide a theoretical foundation for further research on the antibacterial mechanisms of tetramycin.</p>

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Antibacterial mechanism of tetramycin against Pantoea agglomerans, the causal agent of plum bacterial shot-hole disease

  • Houyin Zhou,
  • Kun Guo,
  • Jingzhi Yang,
  • Gul Umair,
  • Xianhui Yin,
  • Yue Ma,
  • Jun Yuan

摘要

The cultivation of plums is significantly endangered by bacterial shot-hole disease, which is caused by Pantoea agglomerans. This study evaluated the antibacterial efficacy of tetramycin against P. agglomerans in comparison with six conventional antibiotics. In vitro assays revealed that 0.3% tetramycin aqueous solutions (AS) exhibited potent inhibitory activity, with a half-maximal effective concentration (EC50) of 1.71 μg/mL. To investigate the mechanistic basis of this activity, alterations in colony morphology, cell membrane permeability, biofilm formation, and energy metabolism were analyzed in tetramycin-treated P. agglomerans. Tetramycin exposure induced significant leakage of electrolytes and macromolecular substances, indicating severe disruption of cell membrane integrity. Concurrently, biofilm formation was markedly suppressed, with an inhibition rate of 51% at EC75. Furthermore, tetramycin altered bacterial metabolic activity, as evidenced by elevated pyruvate accumulation, reduced malate dehydrogenase activity, and decreased ATP levels, suggesting interference with energy metabolism pathways. In conclusion, tetramycin effectively inhibited P. agglomerans growth by disrupting cell membrane stability, suppressing biofilm formation, and impairing energy metabolism. These findings provide a theoretical foundation for further research on the antibacterial mechanisms of tetramycin.