title: A novel W1999S mutation and non-target site resistance impact on acetyl-CoA carboxylase inhibiting herbicides to varying degrees in a UK Lolium multiflorum population.
abstract: BACKGROUND
  Acetyl-CoA carboxylase (ACCase) inhibiting herbicides are important products for the post-emergence control of grass weed species in small grain cereal crops. However, the appearance of resistance to ACCase herbicides over time has resulted in limited options for effective weed control of key species such as Lolium spp. In this study, we have used an integrated biological and molecular biology approach to investigate the mechanism of resistance to ACCase herbicides in a Lolium multiflorum Lam. from the UK (UK21).
  
  
  RESULTS
  The study revealed a novel tryptophan to serine mutation at ACCase codon position 1999 impacting on ACCase inhibiting herbicides to varying degrees. The W1999S mutation confers dominant resistance to pinoxaden and partially recessive resistance to cycloxydim and sethoxydim. On the other hand, plants containing the W1999S mutation were sensitive to clethodim and tepraloxydim. Additionally population UK21 is characterised by other resistance mechanisms, very likely non non-target site based, affecting several aryloxyphenoxyproprionate (FOP) herbicides but not the practical field rate of pinoxaden. The positive identification of wild type tryptophan and mutant serine alleles at ACCase position 1999 could be readily achieved with an original DNA based derived cleaved amplified polymorphic sequence (dCAPS) assay that uses the same PCR product but two different enzymes for positively identifying the wild type tryptophan and mutant serine alleles identified here.
  
  
  CONCLUSIONS
  This paper highlights intrinsic differences between ACCase inhibiting herbicides that could be exploited for controlling ryegrass populations such as UK21 characterised by compound-specific target site and non-target site resistance.
authors.affiliation: Syngenta, Jealott's Hill International Research Centre, Bracknell, United Kingdom. deepak.kaundun@syngenta.com
authors.forename: Shiv Shankhar
authors.initials: SS
authors.lastname: Kaundun
authors.forename: Geraldine C
authors.initials: GC
authors.lastname: Bailly
authors.forename: Richard P
authors.initials: RP
authors.lastname: Dale
authors.forename: Sarah-Jane
authors.initials: SJ
authors.lastname: Hutchings
authors.forename: Eddie
authors.initials: E
authors.lastname: McIndoe
mesh_terms: D000103:Acetyl-CoA Carboxylase / Q000037:antagonists & inhibitors* / Q000235:genetics*; D001483:Base Sequence; D018744:DNA, Plant / Q000235:genetics; D004351:Drug Resistance / Q000235:genetics*; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D005819:Genetic Markers / Q000235:genetics; D006540:Herbicides / Q000494:pharmacology*; D006574:Heterocyclic Compounds, 2-Ring / Q000494:pharmacology; D008129:Lolium / Q000187:drug effects* / Q000201:enzymology / Q000235:genetics; D009154:Mutation; D006113:United Kingdom
chemical_list: D018744:DNA, Plant; D004791:Enzyme Inhibitors; D005819:Genetic Markers; D006540:Herbicides; D006574:Heterocyclic Compounds, 2-Ring; D000103:Acetyl-CoA Carboxylase; C542519:pinoxaden