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研究了采自浙江衢州地区,包括柯城区、衢江区和开化县12个贮藏库的70个柑橘绿霉病菌Penicillium digitatum菌株对抑霉唑和多菌灵的抗性频率、抗性水平及其抗性分子机制。结果表明:柯城区和衢江区的抑霉唑抗性菌株(最低抑制浓度MIC≥0.5μg/mL)的比例分别为77.1%和62.5%,两地抗性菌株的平均EC50值分别为2.07±1.04μg/mL和2.35±0.73μg/mL,分别是当地敏感菌株EC50值的41.4和47.0倍;而采自开化县的菌株均对抑霉唑敏感(MIC≤0.1μg/mL),平均EC50值为0.04±0.02μg/mL。柯城区和衢江区的多菌灵抗性菌株(MIC≥10μg/mL)的比例分别为54.3%和54.2%,而开化县的抗性菌株比例仅为9.1%。即来自柯城和衢江两个柑橘主产区的绿霉病菌群体对抑霉唑和多菌灵的抗性频率均远高于非柑橘主产区的开化县群体,说明抗药性群体的形成与药剂使用历史有关。进一步研究发现,衢州地区柑橘绿霉病菌对抑霉唑的抗性均属于IMZ-R3型,即与抑霉唑靶标基因CYP51B启动子区的插入突变有关,而对多菌灵的抗性则与β-微管蛋白基因的992位核苷酸点突变(T→A)导致对应的200位点的氨基酸突变(F→Y)有关。
The frequency and resistance of imazalil and carbendazim to 70 citruses of Penicillium digitatum from Quzhou, Qujiang and Kaihua counties were investigated. Resistance molecular mechanism. The results showed that the ratios of imazalil resistant strains (minimum inhibitory concentration MIC ≥0.5μg / mL) in Kecheng and Qujiang were 77.1% and 62.5%, respectively. The average EC50 values of the two resistant strains were 2.07 ± 1.04 μg / mL and 2.35 ± 0.73 μg / mL, respectively, which were 41.4 and 47.0 folds of the EC50 value of the local sensitive strains respectively. All the strains collected from Kaihua County were sensitive to imazalil (MIC≤0.1 μg / mL), the average EC50 value 0.04 ± 0.02 μg / mL. The ratios of carbendazim-resistant strains (MIC≥10 μg / mL) in Kecheng and Qujiang districts were 54.3% and 54.2%, respectively, while the proportion of resistant strains in Kaihua County was only 9.1%. That is, the frequency of resistance to imazalil and carbendazim in the populations of M. grisea from the two citrus main producing areas of Kecheng and Qujiang were much higher than that of Kaihua county in the non-citrus main producing areas, indicating the formation of resistant population And pharmaceutical use history. Further study showed that the resistance of citrobacter to imazalil in Quzhou region belonged to IMZ-R3 type, which was related to the insertion mutation of the promoter region of imazalil target gene CYP51B, while the resistance to carbendazim was The 992-nucleotide point mutation (T → A) in the β-tubulin gene results in a mutation at the corresponding 200-site (F → Y).