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抗精噁唑禾草灵和甲基二磺隆看麦娘ACCaseALS基因突变
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引用本文:赵宁,郭文磊,李伟,吕玲玲,刘伟堂,王金信.抗精噁唑禾草灵和甲基二磺隆看麦娘ACCaseALS基因突变.植物保护学报,2017,44(5):833-840
DOI:10.13802/j.cnki.zwbhxb.2017.2016089
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作者单位E-mail
赵宁 山东农业大学植物保护学院, 泰安 271018  
郭文磊 山东农业大学植物保护学院, 泰安 271018  
李伟 山东农业大学植物保护学院, 泰安 271018  
吕玲玲 山东农业大学植物保护学院, 泰安 271018  
刘伟堂 山东农业大学植物保护学院, 泰安 271018  
王金信 山东农业大学植物保护学院, 泰安 271018 wangjx@sdau.edu.cn 
中文摘要:为明确看麦娘Alopecurus aequalis抗性种群YL的靶标抗性机制,采用基因克隆法对看麦娘抗性和敏感种群间乙酰辅酶A羧化酶(ACCase)和乙酰乳酸合成酶(ALS)基因序列进行扩增、克隆和测序,比对二者ACCaseALS基因序列的差异,探寻其产生抗药性突变的基因位点,同时测定该突变型抗性种群YL对不同ACCase和ALS抑制剂类除草剂的交互抗性。结果显示,与看麦娘敏感种群TL相比,抗性种群YL的ACCase基因CT区域第2 041位氨基酸由异亮氨酸(ATT)突变为天冬酰胺酸(AAT),ALS基因Domain A区域第197位氨基酸由脯氨酸(CCC)突变为精氨酸(CGC)。看麦娘抗性种群YL对ACCase抑制剂炔草酯产生了高水平抗性,抗性倍数为43.96,对高效氟吡甲禾灵和精喹禾灵产生了中等水平抗性,抗性倍数分别为18.33和15.87,对唑啉草酯、烯草酮和烯禾啶较敏感;对ALS抑制剂氟唑磺隆产生了低水平抗性,抗性倍数为8.39,对啶磺草胺和咪唑乙烟酸较敏感。表明ACCase基因第2 041位和ALS基因第197位氨基酸突变是导致看麦娘抗性种群YL对精噁唑禾草灵和甲基二磺隆同时产生抗性的重要原因之一。
中文关键词:看麦娘  乙酰辅酶A羧化酶  乙酰乳酸合成酶  基因突变  抗药性
 
Mutations in the acetyl-CoA carboxylase and acetolactate synthase confer resistance to fenoxaprop-P-ethyl and mesosulfuron-methyl in Alopecurus aequalis populations
Author NameAffiliationE-mail
Zhao Ning College of Plant Protection, Shandong Agricultural University, Tai'an 271018, Shandong Province, China  
Guo Wenlei College of Plant Protection, Shandong Agricultural University, Tai'an 271018, Shandong Province, China  
Li Wei College of Plant Protection, Shandong Agricultural University, Tai'an 271018, Shandong Province, China  
Lü Lingling College of Plant Protection, Shandong Agricultural University, Tai'an 271018, Shandong Province, China  
Liu Weitang College of Plant Protection, Shandong Agricultural University, Tai'an 271018, Shandong Province, China  
Wang Jinxin College of Plant Protection, Shandong Agricultural University, Tai'an 271018, Shandong Province, China wangjx@sdau.edu.cn 
Abstract:The objective of this study is to understand the molecular basis of the target-resistance mechanism to fenoxaprop-P-ethyl and mesosulfuron-methyl in Alopecurus aequalis and to find the specific mutation sites in amino acid sequences of acetyl-CoA carboxylase (ACCase) and acetolactate synthase (ALS) in the YL population. Simultaneously, whole-plant dose-response experiments were conducted to evaluate the resistance levels to different ACCase-and ALS-inhibiting herbicides in the resistant A. aequalis population. Fragments encoding the ACCase and ALS were amplified and cloned from susceptible (S) and resistant (R) biotypes of A. aequalis, respectively, and sequenced subsequently. The nucleotide sequence analysis showed that a substitution of isoleucine acid (Ile) 2 041 by asparagine acid (Asn) and 15.87, respectively, and was susceptible to pinoxaden. The YL population showed a low-level resistance to flucarbazone-Na, with a resistance index of 8.39, and was susceptible to pyroxsulam and imazethapyr. This study indicated that the substitutions of isoleucine acid at position 2 041 in the ACCase gene and proline acid at position 197 in the ALS gene might be the important reasons for target-resistance to fenoxaprop-P-ethyl and mesosulfuron-methyl in A. aequalis populations. existed in the CT domain of ACCase gene, and a substitution of proline acid (Pro) 197 by arginine acid (Arg) in the highly conserved region domain A of ALS gene in YL population. The A. aequalis YL population showed a high-level resistance to clodinafop-propargyl with a resistance index of 43.96, and a medium-level resistance to haloxyfop-R-methyl and quizalofop-P-ethyl, with resistance indexes of 18.33 and 15.87, respectively, and was susceptible to pinoxaden. The YL population showed a low-level resistance to flucarbazone-Na, with a resistance index of 8.39, and was susceptible to pyroxsulam and imazethapyr. This study indicated that the substitutions of isoleucine acid at position 2 041 in the ACCase gene and proline acid at position 197 in the ALS gene might be the important reasons for target-resistance to fenoxaprop-P-ethyl and mesosulfuron-methyl in A. aequalis populations.
keywords:Alopecurus aequalis  acetyl-CoA carboxylase  acetolactate synthase  gene mutation  resistance
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