Di Ya-Li, Lu Xiao-Ming, Zhu Zu-Qing, Zhu Fu-Xing
College of Plant Science and Technology, Huazhong Agricultural University, Wuhan, 430070, China.
Plant Dis. 2016 Jul;100(7):1454-1459. doi: 10.1094/PDIS-11-15-1349-RE. Epub 2016 Apr 1.
Previous studies have demonstrated that subtoxic doses of carbendazim have a stimulatory effect on pathogenicity of Sclerotinia sclerotiorum on rapeseed plants. The present study focused on the time-course profile of the stimulatory effect and its relevance to stimulation mechanisms. At 12 h postinoculation (HPI), initial necrotic lesions were visible only for rapeseed leaves treated with carbendazim at 0.2 and 1 μg/ml, whereas no disease symptoms were observed for the nontreated control. At 18 HPI, carbendazim stimulation on pathogenicity was more obvious than at 12 HPI. Study with scanning electron microscopy demonstrated that no discernable differences in the development of disease symptoms could be detected at 8 HPI. However, at 12 HPI, necrotic symptoms of the epidermal cells were apparent only for leaves sprayed with carbendazim. These results indicated that stimulations on pathogenicity occurred in the first 12 h, implying that direct stimulation rather than overcompensation to the disruption of homeostasis was likely to be the underlying mechanism for pathogenicity stimulation. Greenhouse experiments showed that spraying carbendazim at 400 μg/ml on potted rapeseed plants had statistically significant (P < 0.05) stimulations on pathogenicity for inoculations at 1, 3, 5, and 7 days after application (DAA). The stimulation action eventually disappeared for inoculations at 14 DAA. Mycelia grown on potato dextrose agar (PDA) supplemented with carbendazim at 400 μg/ml were more pathogenic than the nontreated control. However, after additional growth of the mycelia on fungicide-free PDA for 2 days, the stimulatory effect disappeared completely, indicating that carbendazim was indispensable for pathogenicity stimulations. Studies on biochemical mechanisms indicated that cell-wall-degrading enzymes such as cellulase, pectinase, and polygalacturonase were not involved in pathogenicity stimulations. These results will advance our understanding of the nature and mechanisms of fungicide stimulation on fungal pathogenicity and, thus, are valuable for judicious applications of fungicides.
先前的研究表明，亚毒性剂量的多菌灵对核盘菌在油菜植株上的致病性具有刺激作用。本研究聚焦于这种刺激作用的时间进程及其与刺激机制的相关性。接种后12小时（hpi），仅在经0.2和1μg/ml多菌灵处理的油菜叶片上可见初始坏死病斑，而未处理的对照未观察到病害症状。接种后18小时，多菌灵对致病性的刺激比接种后12小时更明显。扫描电子显微镜研究表明，接种后8小时在病害症状发展方面未检测到明显差异。然而，接种后12小时，仅喷洒多菌灵的叶片表皮细胞出现坏死症状。这些结果表明，对致病性的刺激发生在最初的12小时内，这意味着直接刺激而非对稳态破坏的过度补偿可能是致病性刺激的潜在机制。温室试验表明，在盆栽油菜植株上以400μg/ml喷洒多菌灵，对施药后1、3、5和7天（DAA）接种的致病性具有统计学显著（P<0.05）的刺激作用。在施药后14天接种时，刺激作用最终消失。在添加400μg/ml多菌灵的马铃薯葡萄糖琼脂（PDA）上生长的菌丝体比未处理的对照更具致病性。然而，在菌丝体在不含杀菌剂的PDA上再生长2天后，刺激作用完全消失，表明多菌灵对于致病性刺激是不可或缺的。生化机制研究表明，纤维素酶、果胶酶和多聚半乳糖醛酸酶等细胞壁降解酶不参与致病性刺激。这些结果将增进我们对杀菌剂刺激真菌致病性的性质和机制的理解，因此对于明智地使用杀菌剂具有重要价值。
