| 吉林狗尾草种群对烟嘧磺隆抗性水平和靶标抗性机理初探 |
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| 引用本文： | 李雯钰,魏守辉,黄红娟,曹 艺,周欣欣,黄兆峰.吉林狗尾草种群对烟嘧磺隆抗性水平和靶标抗性机理初探[J].植物保护,2022,48(6):332-335. |
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| 作者姓名： | 李雯钰 魏守辉 黄红娟 曹 艺 周欣欣 黄兆峰 |
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| 作者单位： | (1. 中国农业科学院植物保护研究所, 北京 100193; 2. 沈阳农业大学生物科学技术学院, 沈阳 110886; 3. 农业农村部农药检定所, 北京 100125) |
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| 基金项目： | 国家重点研发计划（2018YFD0200602）;中央级公益性科研院所基本科研业务费专项（1326036001） |
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| 摘 要： | 为明确吉林省玉米田狗尾草Setaria viridis (L.) Beauv.对烟嘧磺隆的抗药性水平和抗性分子机理,测定了两个抗药性狗尾草种群R1、R2和一个敏感种群S对烟嘧磺隆的抗药水平,并检测了不同种群间乙酰乳酸合成酶(acetolactate synthase,ALS)基因序列差异。结果显示:R1、R2种群抗药性指数分别为21.8和23.9。扩增狗尾草ALS基因序列发现,相较于敏感种群,R1种群在376位点由GAT突变为GAA,R2种群在376位点由GAT突变为GAG,两种突变均导致天冬氨酸替换为谷氨酸(Asp-376-Glu)。表明狗尾草R1和R2种群对烟嘧磺隆产生抗性是由于靶标ALS基因突变导致,研究结果为科学防控抗药性狗尾草种群提供了理论基础。
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| 关 键 词： | 狗尾草 抗药性 乙酰乳酸合成酶 靶标突变 |
| 收稿时间： | 2021/9/28 0:00:00 |
| 修稿时间： | 2021/11/12 0:00:00 |
Preliminary studies on the resistance level and target resistance mechanism of Setaria viridis populations to nicosulfuron in Jilin |
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| LI Wenyu,WEI Shouhui,HUANG Hongjuan,CAO Yi,ZHOU Xinxin,HUANG Zhaofeng.Preliminary studies on the resistance level and target resistance mechanism of Setaria viridis populations to nicosulfuron in Jilin[J].Plant Protection,2022,48(6):332-335. |
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| Authors: | LI Wenyu WEI Shouhui HUANG Hongjuan CAO Yi ZHOU Xinxin HUANG Zhaofeng |
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| Institution: | (1. Institute of Plant Protection, Chinese Academy of Agricultural Sciences, Beijing 100193, China; 2. College of Bioscience and Biotechnology, Shenyang Agricultural University, Shenyang 110886, China; 3. Institute for the Control of Agrochemicals, Ministry of Agriculture and Rural Affairs, Beijing 100125, China) |
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| Abstract: | In order to investigate the resistance level and molecular mechanism of nicosulfuron in Setaria viridis (L.) Beauv., the resistance level of two resistant S. viridis populations (R1 and R2) and a susceptible population (S) to nicosulfuron was determined, and acetolactate synthase (ALS) gene sequences among different populations were also obtained and compared. The results showed that the resistance index of R1 and R2 were 21.8 and 23.9, respectively. Amplification and analysis of ALS gene sequence, the mutation from GAT to GAA at 376 in R1 population, and GAT to GAG at 376 in R2 population, both caused aspartic acid to be replaced by glutamic acid (Asp-376-Glu). The results indicated that the resistant mechanism to nicosulfuron in S. viridis R1 and R2 populations was due to the ALS gene mutation. The above results provide theoretical basis for sustainable management of herbicide-resistant S. viridis population. |
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| Keywords: | Setaria viridis herbicides resistance acetolactate synthetase gene mutation |
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