Mechanisms influencing the evolution of resistance to Qo inhibitor fungicides
Mechanisms influencing the evolution of resistance to Qo inhibitor fungicides
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DOI：
10.1002/ps.565
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发表时间：
2002-09-01
影响因子：
4.1
通讯作者：
McCaffery, A
中科院分区：
文献类型：
--
作者：
Gisi, U;Sierotzki, H;McCaffery, A
通过在Qo位点与细胞色素bc 1酶复合物（复合物III）结合来抑制植物病原体的线粒体呼吸的杀真菌剂（Qo抑制剂，QoI）于1996年首次引入市场。在短时间段后，在一系列重要植物病原体的田间种群中检测到对QoI具有抗性的分离物，所述病原体包括小麦白粉病菌（Blumeria graminis Speer f sp triangulae）、黑星壳菌（Sphaerotheca fuliglium（Schlecht ex Fr）Poll）、葡萄生霜霉病菌（Berk & MA Curtis ex de Bary）Berl & de Toni、古巴霜霉病菌（Pseudoperonospora cubensis（Berk & MA Curtis）Rost）、斐济球腔菌（Mycosphaerella fijiensis Morelet）和苹果黑星病菌（Venturia inaequalis（Cooke）Wint。在大多数情况下，耐药性是由线粒体细胞色素B（cyt B）基因中的点突变引起的，导致第143位氨基酸从甘氨酸变为丙氨酸（G143 A），尽管在许多生物体中已经声称存在其他突变和机制。用含有突变的抗性斐济分枝杆菌分离株的DNA片段转化斐济分枝杆菌敏感的原生质体产生完全抗性的转化体，表明G143 A取代可能是赋予抗性的cyt B基因中最强大的颠换。声称G143 A取代不影响酶的活性，表明抗性个体可能不会遭受显著的适合度惩罚，如在禾本科B小麦赤霉病菌中所证明的。尚不清楚该观察结果是否也适用于表达G143 A置换的其他病原体物种。由于真菌细胞含有大量线粒体，因此必须考虑对QoI的抗性进化中的早期有丝分裂事件，例如突变频率（据称线粒体中的突变频率高于核DNA）、异质细胞阶段中线粒体的细胞内增殖以及突变线粒体的细胞到细胞捐赠。由于cyt B基因位于线粒体基因组中，丝状真菌的抗性遗传预期为非孟德尔遗传，因此在大多数物种中为单亲遗传。在同花受精的小麦B graminis f sp trillium中，敏感和抗性亲本的杂交产生含有敏感或抗性子囊孢子的闭囊霉，并且在F1后代群体中抗性的分离模式为1：1。在异配型真菌V inaequalis中，抗性捐赠是母体的，分离比为1：0。在随机交配种群中，性比（交配型分布）通常假定为1：1。因此，预计敏感个体和抗性个体的总体比例为1：1。QoI抗性的演变主要取决于早期有丝分裂事件;暴露于QoI处理的群体中抗性突变体的选择过程可能遵循与其他杀真菌剂类别中由单核基因控制的抗性相似的机制。它将仍然是重要的是要了解线粒体性质的QoI电阻和因素，如突变，重组，选择和迁移可能会影响QoI电阻在不同的植物病原体的演变。(C)2002年，化学工业协会。
Fungicides inhibiting the mitochondrial respiration of plant pathogens by binding to the cytochrome bc1 enzyme complex (complex III) at the Qo site (Qo inhibitors, QoIs) were first introduced to the market in 1996. After a short time period, isolates resistant to QoIs were detected in field populations of a range of important plant pathogens including Blumeria graminis Speer f sp tritici, Sphaerotheca fuliginea (Schlecht ex Fr) Poll, Plasmopara viticola (Berk & MA Curtis ex de Bary) Berl & de Toni, Pseudoperonospora cubensis (Berk & MA Curtis) Rost, Mycosphaerella fijiensis Morelet and Venturia inaequalis (Cooke) Wint. In most cases, resistance was conferred by a point mutation in the mitochondrial cytochrome b (cyt b) gene leading to an amino-acid change from glycine to alanine at position 143 (G143A), although additional mutations and mechanisms have been claimed in a number of organisms. Transformation of sensitive protoplasts of M fijiensis with a DNA fragment of a resistant M fijiensis isolate containing the mutation yielded fully resistant transformants, demonstrating that the G143A substitution may be the most powerful transversion in the cyt b gene conferring resistance. The G143A substitution is claimed not to affect the activity of the enzyme, suggesting that resistant individuals may not suffer from a significant fitness penalty, as was demonstrated in B graminis f sp tritici. It is not known whether this observation applies also for other pathogen species expressing the G143A substitution. Since fungal cells contain a large number of mitochondria, early mitotic events in the evolution of resistance to QoIs have to be considered, such as mutation frequency (claimed to be higher in mitochondrial than nuclear DNA), intracellular proliferation of mitochondria, in the heteroplasmatic cell stage, and cell to cell donation of mutated mitochondria. Since the cyt b gene is located in the mitochondrial genome, inheritance of resistance in filamentous fungi is expected to be non-Mendelian and, therefore, in most species uniparental. In the isogamous fungus B graminis f sp tritici, crosses of sensitive and resistant parents yielded cleistothecia containing either sensitive or resistant ascospores and the segregation pattern for resistance in the F1 progeny population was 1:1. In the anisogamous fungus V inaequalis, donation of resistance was maternal and the segregation ratio 1:0. In random mating populations, the sex ratio (mating type distribution) is generally assumed to be 1:1. Therefore, the overall proportion of sensitive and resistant individuals in unselected populations is expected to be 1:1. Evolution of resistance to QoIs will depend mainly on early mitotic events; the selection process for resistant mutants in populations exposed to QoI treatments may follow mechanisms similar to those described for resistance controlled by single nuclear genes in other fungicide classes. It will remain important to understand how the mitochondrial nature of QoI resistance and factors such as mutation, recombination, selection and migration might influence the evolution of QoI resistance in different plant pathogens. (C) 2002 Society of Chemical Industry.