杂草对9类常用不同作用机制除草剂的非靶标抗性机制研究进展

除草剂的应用为农业生产带来便利, 但长期、单一使用某一种或相同机制的除草剂也引发了杂草对除草剂的抗性问题。抗性杂草种类逐渐增加, 抗性形成机制复杂, 导致农田杂草的治理难度增加。杂草对除草剂的抗性机制主要分为两种, 一种是除草剂靶标位点基因的突变或过量表达导致的靶标抗性, 另一种是杂草对除草剂吸收、转运、固存和代谢等一个或多个生理过程发生变化导致的非靶标抗性。本文综述了杂草对9类不同作用方式除草剂的非靶标抗性机制的生理、生化和分子基础的研究进展, 以期为抗性杂草综合治理提供参考。     

不同除草剂对11种冬小麦田阔叶杂草的防除效果比较

小麦田除草剂的长期使用,造成麦田杂草群落发生变化。为建立不同区域优势杂草种类的化学防除技术,本研究采用室内盆栽法测定了14种除草剂对11种冬小麦田阔叶杂草的防除效果。结果表明,灭草松可以较好地防除冬小麦田野老鹳草、牛繁缕、大巢菜、紫堇、小藜、阿拉伯婆婆纳、播娘蒿、猪殃殃、麦家公等阔叶杂草;吡草醚对野老鹳草、牛繁缕、小藜、阿拉伯婆婆纳、播娘蒿、猪殃殃、麦家公、荠菜等8种杂草防效突出。辛酰溴苯腈可很好地防除牛繁缕、大巢菜、小藜、阿拉伯婆婆纳、播娘蒿、麦家公等6种阔叶杂草;唑草酮对野老鹳草、牛繁缕、阿拉伯婆婆纳、播娘蒿、猪殃殃等5种杂草防效突出。这4种除草剂及其适用浓度与其他供试药剂相比杀草谱更为广泛,对阔叶杂草防效较好。根据不同区域优势杂草种类,合理选用高效除草剂进行防除。     

杂草对除草剂非靶标抗性机理研究进展

随着除草剂的大面积持续使用,近年来抗性杂草种类增多,危害面积不断增加,危害程度逐渐加重。杂草对除草剂抗性问题业已成为威胁全球粮食安全的关键问题之一。杂草对除草剂的抗药机制主要分为靶标抗性和非靶标抗性,非靶标抗性主要包括对除草剂解毒能力增强、屏蔽作用或与作用位点的隔离作用等机理。本文主要对除草剂的非靶标抗性机制中的P450s、GSTs、ABC转运蛋白和谷胱甘肽转运体等进行综述,并对非靶标抗性机制研究前景进行展望。     

4种芽前除草剂防除直播小白菜田杂草的效果及其安全性

采用田间试验方法研究了33%二甲戊灵乳油、96%精异丙甲草胺乳油、50%敌草胺水分散粒剂和90%禾草丹乳油4种芽前除草剂防除直播小白菜田杂草效果及其安全性,筛选出了适于直播小白菜田的芽前除草剂。结果表明,药后35d,33%二甲戊灵乳油有效用量371.25~742.5g/hm2、96%精异丙甲草胺乳油864~1 080g/hm2和90%禾草丹乳油1 687.5~2 025g/hm2处理无论是总草株防效还是鲜重防效均在94.27%以上,其次是50%敌草胺水分散粒剂750~1 500g/hm2处理,防效为85.62%~90.54%。33%二甲戊灵乳油各供试剂量虽对小白菜的出苗没有影响,但对小白菜的生长有一定影响,表现为地上部株高和鲜重受抑制;其他3个供试除草剂各剂量处理对小白菜出苗和生长安全。从除草效果和安全性两方面综合考虑,推荐96%精异丙甲草胺乳油864~1 080g/hm2和90%禾草丹乳油1 687.5~2 025g/hm2用于小白菜田芽前防除杂草。     

Evaluation of novel sulfonylurea derivatives with a fused heterocyclic moiety as paddy herbicides that control sulfonylurea‐resistant weeds

Herbicidal activity and acetolactate synthase (ALS) inhibition of sulfonylurea derivatives with a fused heterocyclic moiety bonded to a sulfonyl group were investigated. Some compounds that had an imidazo[1,2‐b]pyridazine moiety substituted at the 2‐position by chlorine or methyl controlled sulfonylurea‐resistant (SU‐R) weeds and showed inhibitory activity to ALS prepared from SU‐R Schoenoplectus juncoides shoot. There was a correlation between in vitro and whole‐plant herbicidal activity of the compounds mentioned above against SU‐R Schoenoplectus juncoides. Among them 1‐(2‐chloro‐6‐propylimidazo[1,2‐b]pyridazin‐3‐ylsulfonyl)‐3‐(4,6‐dimethoxypyrimidin‐2‐yl)urea, propyrisulfuron, was selected for further evaluation. Propyrisulfuron effectively controlled paddy weeds at doses of 70 and 140 g a.i. ha^?1 with good rice selectivity in a field trial.     

Molecular characterisation of resistance to ALS-inhibiting herbicides in Hordeum leporinum biotypes

BACKGROUND: The acetolactate synthase (ALS)-inhibiting herbicide sulfosulfuron is registered in Australia for the selective control of Hordeum leporinum Link. in wheat crops. This herbicide failed to control H. leporinum on two farms in Western Australia on its first use. This study aimed to determine the level of resistance of three H. leporinum biotypes, identify the biochemical and molecular basis and develop molecular markers for diagnostic analysis of the resistance. RESULTS: Dose-response studies revealed very high level (>340-fold) resistance to the sulfonylurea herbicides sulfosulfuron and sulfometuron. In vitro ALS assays revealed that resistance was due to reduced sensitivity of the ALS enzyme to herbicide inhibition. This altered ALS sensitivity in the resistant biotypes was found to be due to a mutation in the ALS gene resulting in amino acid proline to serine substitution at position 197. In addition, two- to threefold higher ALS activities were consistently found in the resistant biotypes, compared with the known susceptible biotype. Two cleaved amplified polymorphic sequence (CAPS) markers were developed for diagnostic testing of the resistant populations. CONCLUSION: This study established the first documented case of evolved ALS inhibitor resistance in H. leporinum and revealed that the molecular basis of resistance is due to a Pro to Ser mutation in the ALS gene.     

Multiple resistance across glufosinate,glyphosate, paraquat and ACCase‐inhibiting herbicides in an Eleusine indica population

An Eleusine indica population was previously reported as the first global case of field‐evolved glufosinate resistance. This study re‐examines glufosinate resistance and investigates multiple resistance to other herbicides in the population. Dose–response experiments with glufosinate showed that the resistant population is 5‐fold and 14‐fold resistant relative to the susceptible population, based on GR₅₀ and LD₅₀ R/S ratio respectively. The selected glufosinate‐resistant subpopulation also displayed a high‐level resistance to glyphosate, with the respective GR₅₀ and LD₅₀ R/S ratios being 12‐ and 144‐fold. In addition, the subpopulation also displayed a level of resistance to paraquat and ACCase‐inhibiting herbicides fluazifop‐P‐butyl, haloxyfop‐P‐methyl and butroxydim. ACCase gene sequencing revealed that the Trp‐2027‐Cys mutation is likely responsible for resistance to the ACCase inhibitors examined. Here, we confirm glufosinate resistance and importantly, we find very high‐level glyphosate resistance, as well as resistance to paraquat and ACCase‐inhibiting herbicides. This is the first confirmed report of a weed species that evolved multiple resistance across all the three non‐selective global herbicides, glufosinate, glyphosate and paraquat.     

Evolving understanding of the evolution of herbicide resistance

A greater number of, and more varied, modes of resistance have evolved in weeds than in other pests because the usage of herbicides is far more extensive than the usage of other pesticides, and because weed seed output is so great. The discovery and development of selective herbicides are more problematic than those of insecticides and fungicides, as these must only differentiate between plant and insect or pathogen. Herbicides are typically selective between plants, meaning that before deployment there are already some crops possessing natural herbicide resistance that weeds could evolve. The concepts of the evolution of resistance and the mechanisms of delaying resistance have evolved as nature has continually evolved new types of resistance. Major gene target‐site mutations were the first types to evolve, with initial consideration devoted mainly to them, but slowly ‘creeping’ resistance, gradually accruing increasing levels of resistance, has become a major force owing to an incremental accumulation of genetic changes in weed populations. Weeds have evolved mechanisms unknown even in antibiotic as well as other drug and pesticide resistances. It is even possible that cases of epigenetic ‘remembered’ resistances may have appeared. Copyright © 2009 Society of Chemical Industry     

Identification of a target‐site mutation conferring resistance to triazine herbicides in oriental mustard (Sisymbrium orientale L.) from Australia

In southern Australia, oriental mustard (Sisymbrium orientale) has been controlled successfully by triazine herbicides for several decades. The screening of 40 populations that were collected from the southern grain belt of Australia during 2010 and 2013 for resistance to six different herbicides (glyphosate, diflufenican, imazamox, chlorsulfuron, atrazine and 2,4‐dichlorophenoxyacetic acid) identified two oriental mustard populations as highly resistant to atrazine. Compared to the known oriental mustard‐susceptible populations (S1 and S2), these two resistant populations (P17 and P18) from near Horsham, Victoria, Australia, were 311‐ and 315‐fold resistant to atrazine, as determined by a comparison of the LD₅₀ values. However, there was no resistance to diuron detected in these populations. Sequencing of the chloroplast psbA gene identified a missense mutation of serine 264 to glycine in both herbicide‐resistant oriental mustard populations, which is known to confer high‐level atrazine resistance in other species.     

Cross-resistance patterns to ACCase-inhibiting herbicides conferred by mutant ACCase isoforms in Alopecurus myosuroides Huds. (black-grass), re-examined at the recommended herbicide field rate

BACKGROUND: Target‐site‐based resistance to acetyl‐CoA carboxylase (ACCase) inhibitors in Alopecurus myosuroides Huds. is essentially due to five substitutions (Isoleucine‐1781‐Leucine, Tryptophan‐2027‐Cysteine, Isoleucine‐2041‐Asparagine, Aspartate‐2078‐Glycine, Glycine‐2096‐Alanine). Recent studies suggested that cross‐resistance patterns associated with each mutation using a seed‐based bioassay may not accurately reflect field resistance. The authors aimed to connect the presence of mutant ACCase isoform(s) in A. myosuroides with resistance to five ACCase inhibitors (fenoxaprop, clodinafop, haloxyfop, cycloxydim, clethodim) sprayed at the recommended field rate. RESULTS: Results from spraying experiments and from seed‐based bioassays were consistent for all mutant isoforms except the most widespread, Leucine‐1781. In spraying experiments, Leucine‐1781 ACCase conferred resistance to clodinafop and haloxyfop. Some plants containing Leucine‐1781 or Alanine‐2096 ACCase, but not all, were also resistant to clethodim. CONCLUSION: Leucine‐1781, Cysteine‐2027, Asparagine‐2041 and Alanine‐2096 ACCases confer resistance to fenoxaprop, clodinafop and haloxyfop at field rates. Leucine‐1781 ACCase also confers resistance to cycloxydim at field rate. Glycine‐2078 ACCase confers resistance to all five herbicides at field rates. Only Glycine‐2078 ACCase confers clethodim resistance under optimal application conditions. It may be that Leucine‐1781 and Alanine‐2096 ACCases may also confer resistance to clethodim in the field if the conditions are not optimal for herbicide efficacy, or at reduced clethodim field rates. Copyright © 2008 Society of Chemical Industry