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由细胞骨架蛋白微管蛋白的自发突变引起的除草剂抗性。

Herbicide resistance caused by spontaneous mutation of the cytoskeletal protein tubulin.

作者信息

Anthony R G, Waldin T R, Ray J A, Bright S W, Hussey P J

机构信息

School of Biological Sciences, Royal Holloway University of London, Surrey, UK.

出版信息

Nature. 1998 May 21;393(6682):260-3. doi: 10.1038/30484.

Abstract

The dinitroaniline herbicides (such as trifluralin and oryzalin) have been developed for the selective control of weeds in arable crops. However, prolonged use of these chemicals has resulted in the selection of resistant biotypes of goosegrass, a major weed. These herbicides bind to the plant tubulin protein but not to mammalian tubulin. Here we show that the major alpha-tubulin gene of the resistant biotype has three base changes within the coding sequence. These base changes swap cytosine and thymine, most likely as the result of the spontaneous deamination of methylated cytosine. One of these base changes causes an amino-acid change in the protein: normal threonine at position 239 is changed to isoleucine. This position is close to the site of interaction between tubulin dimers in the microtubule protofilament. We show that the mutated gene is the cause of the herbicide resistance by using it to transform maize and confer resistance to dinitroaniline herbicides. Our results provide a molecular explanation for the resistance of goosegrass to dinitroanaline herbicides, a phenomenon that has arisen, and been selected for, as a result of repeated exposure to this class of herbicide.

摘要

二硝基苯胺类除草剂(如氟乐灵和安磺灵)已被开发用于选择性防治耕地作物中的杂草。然而,长期使用这些化学物质导致了主要杂草马唐抗药生物型的产生。这些除草剂与植物微管蛋白结合,但不与哺乳动物微管蛋白结合。我们在此表明,抗药生物型的主要α-微管蛋白基因在编码序列内有三个碱基变化。这些碱基变化使胞嘧啶和胸腺嘧啶互换,很可能是甲基化胞嘧啶自发脱氨的结果。其中一个碱基变化导致蛋白质中的一个氨基酸变化:第239位的正常苏氨酸变为异亮氨酸。该位置靠近微管原丝中微管蛋白二聚体的相互作用位点。我们通过将其用于转化玉米并赋予对二硝基苯胺类除草剂的抗性,表明突变基因是除草剂抗性的原因。我们的结果为马唐对二硝基苯胺类除草剂的抗性提供了分子解释,这种现象是由于反复接触此类除草剂而产生并被选择出来的。

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