Wang Hua, Liu Wei, Mao Yiru, Mi Qianqian, Wang Shuchang, Tan Yunxiao, Huang Ying'ao, Wang Nana, Yan Xia, Huang Lili
State Key Laboratory for Crop Stress Resistance and High-Efficiency Production, College of Plant Protection, Northwest A&F University, Yangling, P. R. China.
Laboratory of Natural Products Pesticides, College of Plant Protection, Southwest University, Chongqing, P. R. China.
Pest Manag Sci. 2025 Sep;81(9):5835-5847. doi: 10.1002/ps.8939. Epub 2025 May 30.
Streptothricins (STs) are microbial-derived compounds effective against Pseudomonas syringae pv. actinidiae (Psa), the causal agent of kiwifruit bacterial canker. However, the risk of resistance development and underlying mechanisms in Psa remain unclear. This study aims to establish baseline sensitivity of Psa to STs, characterize resistance-associated phenotypes, and identify molecular resistance mechanisms to inform sustainable STs use in agriculture.
Sensitivity testing of 186 Psa isolates from Chinese kiwifruit-producing regions revealed no naturally resistant strains, with a mean baseline half-maximal effective concentration (EC) of 1.000 ± 0.240 μg mL for STs. Laboratory-induced STs-resistant mutants (R-Psa) exhibited significant fitness costs, slower growth rates, impaired motility, and complete loss of virulence in planta, with no leaf necrosis observed in inoculated kiwifruit. Cross-resistance assays showed no or low cross-resistance to streptomycin, tetramycin, copper hydroxide, and kasugamycin. Molecular analyses identified a GNAT-family acetyltransferase, P-SatA, as the key resistance determinant: overexpression of P-SatA reduced STs sensitivity by 100-fold, while gene deletion restored wild-type sensitivity. In vitro validation confirmed P-SatA inactivates STs via acetylation, abolishing antibacterial activity.
This study establishes that STs resistance in Psa is mediated by P-SatA-dependent acetylation, with resistant strains incurring substantial fitness penalties that limit their environmental competitiveness. The absence of natural resistance and low cross-resistance to other pesticides highlight STs as a sustainable option for kiwifruit canker management. These findings advance our understanding of metabolic resistance mechanisms in plant pathogens and provide a scientific basis for optimizing STs application to mitigate resistance risks. © 2025 Society of Chemical Industry.
链丝菌素（STs）是一种微生物来源的化合物，对猕猴桃细菌性溃疡病的病原菌——丁香假单胞菌猕猴桃致病变种（Psa）有效。然而，Psa中耐药性产生的风险及潜在机制仍不清楚。本研究旨在确定Psa对STs的基线敏感性，表征与抗性相关的表型，并确定分子抗性机制，以为农业中可持续使用STs提供依据。
对来自中国猕猴桃产区的186株Psa分离株进行敏感性测试，结果显示没有天然抗性菌株，STs的平均基线半数最大有效浓度（EC）为1.000±0.240μg/mL。实验室诱导的STs抗性突变体（R-Psa）表现出显著的适合度代价，生长速率较慢，运动能力受损，并且在植物体内毒力完全丧失，接种的猕猴桃中未观察到叶片坏死。交叉抗性试验表明，对链霉素、四霉素、氢氧化铜和春雷霉素没有或只有低交叉抗性。分子分析确定了一种GNAT家族乙酰转移酶P-SatA是关键的抗性决定因素：P-SatA的过表达使对STs的敏感性降低了100倍，而基因缺失则恢复了野生型敏感性。体外验证证实P-SatA通过乙酰化使STs失活，从而消除抗菌活性。
本研究确定Psa中的STs抗性是由P-SatA依赖性乙酰化介导的，抗性菌株会受到显著的适合度惩罚，这限制了它们在环境中的竞争力。不存在天然抗性以及对其他农药的低交叉抗性突出了STs作为猕猴桃溃疡病管理的可持续选择。这些发现推进了我们对植物病原体代谢抗性机制的理解，并为优化STs应用以降低抗性风险提供了科学依据。©2025化学工业协会。
