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美国威斯康星州疫霉属致病疫霉克隆谱系US-23引起番茄和马铃薯晚疫病的首次报道

First Report of Late Blight Caused by Phytophthora infestans Clonal Lineage US-23 on Tomato and Potato in Wisconsin, United States.

作者信息

Gevens A J, Seidl A C

机构信息

Department of Plant Pathology, University of Wisconsin, Madison, 53706.

出版信息

Plant Dis. 2013 Jun;97(6):839. doi: 10.1094/PDIS-09-12-0821-PDN.

DOI:10.1094/PDIS-09-12-0821-PDN
PMID:30722586
Abstract

Tomato (Solanum lycopersicum) and potato (S. tuberosum) crops are grown on over 67,000 acres (27,114 ha) in Wisconsin annually. Late blight, caused by Phytophthora infestans (Mont.) deBary, is a potentially devastating disease that affects tomato and potato crops in Wisconsin every few years when inoculum is introduced and weather conditions favor disease. Incidence and severity of late blight are highly variable in these few years due to differences in pathogen clonal lineages, their timing and means of introduction, and weather conditions. Prevention of this disease through preventative application of fungicides can cost producers millions of dollars per year in additional chemical, fuel, and labor expenses. In 2009, late blight caused by P. infestans clonal lineage US-23 was observed on potato very late in the season in Vernon County, southwestern Wisconsin, in very low incidence and severity. In 2010, US-23 again appeared but on tomato in two southeastern Wisconsin counties, Waukesha and Ozaukee, again in low incidence and severity. Clonal lineages of P. infestans documented in Wisconsin in previous epidemics included US-8 in the mid-1990s and US-1 in the 1970s. Populations of P. infestans in the United States have recently undergone significant genetic change, resulting in isolates with unique clonal lineages and epidemiological characteristics (1). Foliar symptoms included water-soaked to dark brown circular lesions with pale green haloes accompanied by white pathogen sporulation. On tomato fruit, lesions were firm, sunken, and brown. Isolates of P. infestans were generated from field-infected tomato and potato foliar and fruit tissues collected by the authors and professional crop consultants. In initial pathogen confirmation analysis in 2009, three isolates of P. infestans were generated from one potato plant exhibiting multiple lesions from one of eight fields tested by placing infected leaf excisions onto Rye A agar amended with rifampicin and ampicillin. Axenic, single zoospore-derived cultures of isolates were generated from parent cultures and maintained on Rye A agar for further characterization. In 2010, three US-23 isolates were recovered from three locations (two counties), out of 20 fields tested. Mycelium was coenocytic with hyphal diameter of 5 to 8 μm (n = 50). Sporangia were limoniform or ovoid, semi to fully papillate, caducous, had short pedicels, and were 26.16 μm high × 18.17 μm wide (n = 50). The average length/width ratio was 1.42. Allozyme banding patterns at the glucose-6-phosphate isomerase (Gpi) locus indicated a 100/100 profile, consistent with the US-23 clonal lineage (3) Mating type assays confirmed the isolates to be A1 and in vitro intermediate mefenoxam sensitivity was observed (4). Genomic DNA was extracted with a phenol/chloroform/isoamyl alcohol solution and RFLP analysis was performed using the RG-57 probe on a representative isolate and resulted in banding patterns consistent with US-23 (2,3). The P. infestans clonal lineage US-23 was present in epidemics in 2009 and 2010 in the United States. Disease symptoms associated with US-23 were observed exclusively on potato in 2009 and on tomato in 2010 in Wisconsin. To our knowledge, this is the first report of P. infestans clonal lineage US-23 causing late blight on tomato and potato in Wisconsin and represents a change in the composition of the pathogen population from previous epidemic years. References: (1) K. Deahl. (Abstr.) Phytopathology 100:S161, 2010. (2) S. B. Goodwin et al. Curr. Genet. 22:107, 1992. (3) Hu et al. Plant Dis. 96:1323, 2012. (4) A. C. Seidl and A. J. Gevens. (Abstr.) Phytopathology 101(suppl.):S162, 2011.

摘要

番茄(茄属番茄种)和马铃薯(茄属马铃薯种)作物在威斯康星州每年的种植面积超过67000英亩(27114公顷)。由致病疫霉(蒙氏致病疫霉)引起的晚疫病是一种潜在的毁灭性病害,每隔几年,当接种体传入且天气条件有利于病害发生时,就会影响威斯康星州的番茄和马铃薯作物。在这几年中,由于病原菌克隆谱系、其传入的时间和方式以及天气条件的差异,晚疫病的发病率和严重程度变化很大。通过预防性施用杀菌剂来预防这种病害,每年会使生产者在额外的化学品、燃料和劳动力费用上花费数百万美元。2009年,在威斯康星州西南部弗农县马铃薯生长季节末期,观察到由致病疫霉克隆谱系US - 23引起的晚疫病,发病率和严重程度都很低。2010年,US - 23再次出现,但出现在威斯康星州东南部的沃基沙和奥佐基两个县的番茄上,发病率和严重程度同样很低。在威斯康星州以前的疫情中记录的致病疫霉克隆谱系包括20世纪90年代中期的US - 8和70年代的US - 1。美国的致病疫霉种群最近发生了显著的遗传变化,产生了具有独特克隆谱系和流行病学特征的分离株(1)。叶部症状包括水渍状至深褐色圆形病斑,周围有浅绿色晕圈,并伴有白色病原菌孢子形成。在番茄果实上,病斑坚硬、凹陷且呈褐色。致病疫霉分离株是从作者和专业作物顾问采集的田间感染的番茄和马铃薯叶部及果实组织中获得的。在2009年最初的病原菌确认分析中,从一株表现出多个病斑的马铃薯植株上获得了3个致病疫霉分离株,该植株来自8个测试田中的一块,将感染的叶片切块放在添加了利福平和平氨苄青霉素的黑麦A琼脂上。从亲代培养物中获得了分离株的无菌、单游动孢子衍生培养物,并在黑麦A琼脂上保存以进行进一步鉴定。2010年,在测试的20块田中,从3个地点(2个县)分离出了3个US - 23分离株。菌丝体多核,菌丝直径为5至8μm(n = 50)。孢子囊柠檬形或卵形,半乳头状至完全乳头状,脱落,有短梗,高26.16μm×宽18.17μm(n = 50)。平均长宽比为1.42。葡萄糖 - 6 - 磷酸异构酶(Gpi)位点的等位酶带型显示为100/100图谱,与US - 23克隆谱系一致(3)。交配型测定证实分离株为A1型,并观察到其对甲霜灵的体外敏感性为中等(4)。用酚/氯仿/异戊醇溶液提取基因组DNA,并使用RG - 57探针在一个代表性分离株上进行RFLP分析,结果得到的带型与US - 23一致(2,3)。致病疫霉克隆谱系US - 23在2009年和2010年在美国的疫情中出现。2009年在威斯康星州仅在马铃薯上观察到与US - 23相关的病害症状,2010年则仅在番茄上观察到。据我们所知,这是致病疫霉克隆谱系US - 23在威斯康星州导致番茄和马铃薯晚疫病的首次报道,代表了病原菌种群组成与以往疫情年份相比发生了变化。参考文献:(1)K. Deahl.(摘要)植物病理学100:S161,2010。(2)S. B. Goodwin等人。当代遗传学22:107,1992。(3)Hu等人。植物病害96:1323,2012。(4)A. C. Seidl和A. J. Gevens。(摘要)植物病理学101(增刊):S162,2011。

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