Bolton M D, Neher O T
USDA-ARS, Northern Crop Science Laboratory, Fargo, ND 58102.
The Amalgamated Sugar Company LLC, Boise, ID 83709.
Plant Dis. 2014 Jul;98(7):1004. doi: 10.1094/PDIS-12-13-1217-PDN.
The $2.1 billion United States sugar beet (Beta vulgaris L.) industry is the primary provider of domestic sucrose. Sugar beet powdery mildew is caused by Erysiphe polygoni DC and occurs principally in sugar beet growing regions in the western United States. In these regions, the quinone outside inhibitor (QI) fungicides pyraclostrobin (Headline, BASF, NC) and trifloxystrobin (Gem, Bayer Crop Science, NC) have been important tools to manage powdery mildew since registration in 2002 and 2005, respectively. However, researchers in Idaho reported poor disease management despite QI application starting in 2011. In 2013, a research plot near Parma, ID, containing natural powdery mildew infection received treatments of pyraclostrobin, trifloxystrobin, or was untreated (control). Since there was no significant reduction in disease levels between QI-treated blocks and untreated control blocks, experiments were conducted to clone a partial fragment of the E. polygoni cytochrome b (cytb) gene to gain insight into the molecular basis of QI resistance in this pathosystem. The primers MDB-920 (5'-CACATCGGAAGAGGTTTATA-3') and MDB-922 (5'-GGTATAGATCTTAATATAGCATAG-3') were designed based on consensus sequences of several fungal cytb genes obtained from GenBank (data not presented) and used to amplify a 575-bp fragment of the E. polygoni cytb gene using DNA isolated from 12 infected leaf samples collected in September 2013 from the Parma research plot. Each sample consisted of three leaves harvested from three plants (one leaf per plant) in an experimental block. All DNA extraction, PCR, and sequencing procedures were as described previously (1). PCR products derived from six QI-treated samples and six untreated samples were sequenced directly. Without exception, all QI-treated samples harbored a point mutation at nucleotide position 143 that encoded a G143A mutation compared with cytb sequence from untreated samples. The two identified cytb haplotypes have been deposited in GenBank under accession numbers KF925325 and KF925326. This is the first report of QI resistance and the associated cytb G143A mutation in E. polygoni. The G143A mutation has been reported in most QI-resistant pathogens to date (2). When the G143A mutation dominates in a pathogen population, there is a consistent association with a loss of disease management despite QI application (3). Careful monitoring and judicious use of QI fungicides will be necessary to ensure QI fungicides remain efficacious for sugar beet powdery mildew management in the United States. References: (1) M. D. Bolton et al. Pest Manag. Sci. 69:35, 2013. (2) N. Fisher and B. Meunier. FEMS Yeast Res. 8:183, 2008. (3) U. Gisi et al. Pest Manag. Sci. 58:859, 2002.
价值21亿美元的美国甜菜（Beta vulgaris L.）产业是国内蔗糖的主要供应者。甜菜白粉病由蓼白粉菌（Erysiphe polygoni DC）引起，主要发生在美国西部的甜菜种植区。在这些地区，自2002年和2005年分别登记以来，醌外抑制剂（QI）类杀菌剂吡唑醚菌酯（Headline，巴斯夫公司，北卡罗来纳州）和肟菌酯（Gem，拜耳作物科学公司，北卡罗来纳州）一直是防治白粉病的重要工具。然而，爱达荷州的研究人员报告称，自2011年开始使用QI类杀菌剂以来，病害防治效果不佳。2013年，在爱达荷州帕尔马附近的一块含有自然白粉病感染的试验田中，对吡唑醚菌酯、肟菌酯进行了处理，或不进行处理（对照）。由于QI处理区和未处理对照区之间的病害水平没有显著降低，因此进行了实验，以克隆蓼白粉菌细胞色素b（cytb）基因的部分片段，从而深入了解该病原体系中QI抗性的分子基础。引物MDB - 920（5'-CACATCGGAAGAGGTTTATA-3'）和MDB - 922（5'-GGTATAGATCTTAATATAGCATAG-3'）是根据从GenBank获得的几个真菌cytb基因的共有序列设计的（数据未列出），并用于使用从2013年9月从帕尔马试验田采集的12个感染叶片样本中分离的DNA扩增蓼白粉菌cytb基因的一个575 bp片段。每个样本由从试验小区的三株植物上收获的三片叶子组成（每株植物一片叶子）。所有DNA提取、PCR和测序程序均如先前所述（1）。直接对来自六个QI处理样本和六个未处理样本的PCR产物进行测序。无一例外，与未处理样本的cytb序列相比，所有QI处理样本在核苷酸位置143处都存在一个点突变，该突变编码G143A突变。鉴定出的两种cytb单倍型已保存在GenBank中，登录号为KF925325和KF925326。这是关于蓼白粉菌中QI抗性及相关cytb G143A突变的首次报道。迄今为止，大多数对QI产生抗性的病原体中都报道了G143A突变（2）。当G143A突变在病原体群体中占主导时，尽管使用了QI类杀菌剂，但病害防治效果仍会持续下降（3）。为确保QI类杀菌剂在美国甜菜白粉病防治中继续有效，有必要进行仔细监测并明智使用。参考文献：（1）M. D. Bolton等人，《害虫管理科学》69：35，2013年。（2）N. Fisher和B. Meunier，《FEMS酵母研究》8：183，2008年。（3）U. Gisi等人，《害虫管理科学》58：859，2002年。
