Main ConclusionThis is a first report of an Ala-205-Phe substitution in acetolactate synthase conferring resistance to imidazolinone, sulfonylurea, triazolopyrimidines, sulfonylamino-carbonyl-triazolinones, and pyrimidinyl (thio) benzoate herbicides.Resistance to acetolactate synthase (ALS) and photosystem II inhibiting herbicides was confirmed in a population of allotetraploid annual bluegrass (Poa annua L.; POAAN-R3) selected from golf course turf in Tennessee. Genetic sequencing revealed that seven of eight POAAN-R3 plants had a point mutation in the psbA gene resulting in a known Ser-264-Gly substitution on the D1 protein. Whole plant testing confirmed that this substitution conferred resistance to simazine in POAAN-R3. Two homeologous forms of the ALS gene (ALSa and ALSb) were detected and expressed in all POAAN-R3 plants sequenced. The seven plants possessing the Ser-264-Gly mutation conferring resistance to simazine also had a homozygous Ala-205-Phe substitution on ALSb, caused by two nucleic acid substitutions in one codon. In vitro ALS activity assays with recombinant protein and whole plant testing confirmed that this Ala-205-Phe substitution conferred resistance to imidazolinone, sulfonylurea, triazolopyrimidines, sulfonylamino-carbonyl- triazolinones, and pyrimidinyl (thio) benzoate herbicides. This is the first report of Ala-205-Phe mutation conferring wide spectrum resistance to ALS inhibiting herbicides.Electronic supplementary materialThe online version of this article (doi:10.1007/s00425-015-2399-9) contains supplementary material, which is available to authorized users.
Annual bluegrass resistance to inhibitors of acetolactate synthase (ALS) and photosystem II (PSII) in managed turf has been confirmed in the southeastern United States. A biotype of annual bluegrass that had developed resistance (R) to the PSII inhibitor simazine was not controlled by POST applications of foramsulfuron or trifloxysulfuron in 2011 or 2012. In whole plant dose-response experiments, trifloxysulfuron, simazine, and indaziflam controlled a susceptible (S) population of annual bluegrass > 91% when applied POST to nontillering plants. However, trifloxysulfuron applications at 3.5 to 223 g ai ha−1only controlled R annual bluegrass ≤ 40%. Similarly, simazine at 140 to 9,000 g ai ha−1only controlled R annual bluegrass ≤ 20%. R annual bluegrass plants were more tolerant to indaziflam applied POST to leaf stage plants prior to tillering, as rates > 100 g ai ha−1were needed to control R annual bluegrass ≥ 96%. No differences in the activity of ALS in R and S plants exposed to increasing foramsulfuron concentrations from 0 to 100 µM were detected suggesting that nontarget mechanisms could explain reduced efficacy of POST herbicide applications in whole plant dose-response experiments. Applications of indaziflam (35 to 70 g ha−1) and oxadiazon (2,240 to 4,500 g ai ha−1) effectively controlled R annual bluegrass when applied PRE. This biotype of R annual bluegrass is the first reported instance of a weed developing resistance to multiple modes of action in managed turf. Education is needed among turf managers regarding the consequences of exclusive use of the same herbicides for annual bluegrass control leading to the onset of herbicide resistance.
A population of junglerice from Sunflower County, MS, exhibited resistance to fenoxaprop-P-ethyl. An 11-fold difference in ED50 (the effective dose needed to reduce growth by 50%) values was observed when comparing the resistant population (249 g ae ha–1) with susceptible plants (20 g ae ha–1) collected from a different field. The resistant population was controlled by clethodim and sethoxydim at the field rate. Sequencing of the acetyl coenzyme A carboxylase, which encodes the enzyme targeted by fenoxaprop-P-ethyl, did not reveal the presence of any known resistance-conferring point mutations. An enzyme assay confirmed that the acetyl coenzyme A carboxylase in the resistant population is herbicide sensitive. Further investigations with two cytochrome P450 inhibitors, malathion and piperonyl butoxide, and a glutathione-S-transferase inhibitor, 4-chloro-7-nitrobenzofurazan, did not indicate involvement of any metabolic enzymes inhibited by these compounds. The absence of a known target-site point mutation and the sensitivity of the ACCase enzyme to herbicide show that fenoxaprop-P-ethyl resistance in this population is due to a non–target-site mechanism or mechanisms.
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