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A New Target Site Mutation Conferring Broad Spectrum Resistance to ALS-Inhibiting Herbicides

J.T. Brosnan, J.J. Vargas, G.K. Breeden, L. Grier, S. Tresch, R.A. Aponte, and M. LaForest (2015) A New Target Site Mutation Conferring Broad Spectrum Resistance to ALS-Inhibiting Herbicides, poster at CWSS-SCM Annual Meeting, Edmonton, Canada, November 2015.


Annual bluegrass (Poa annua L.) is a problematic weed of crop and non-cropping systems globally. In turfgrass, there are more reports of herbicide resistance in annual bluegrass than any other weed species with resistance to inhibitors of acetolactate synthase (ALS), photosystem II (PSII), cellular mitosis, and enolpyruvylshikimate-3-phosphate (EPSP) synthase all documented. However, there are limited reports of multiple-coexisting resistances in annual bluegrass. A biotype of annual bluegrass on a golf course (POAAN-R3; Memphis, Tennessee USA) evolved resistance to applications of simazine and trifloxysulfuron. Under greenhouse conditions, treatment with these herbicides at 8x labeled rates controlled plants ≤ 40%. We hypothesized that POAAN-R3 would contain multiple target site mutations conferring resistance to ALS and PSII inhibiting herbicides. Seven of eight R plants had Ser-264-Gly substitution on psbA that conferred resistance to simazine. Two homeologs of ALS gene present in all R plants, ALSa and ALSb with coding and amino acid sequence identity of 96.2 and 98.0%, respectively. Plants expressing the Ser-264-Gly mutation also had a homozygous Ala-205-Phe substitution on ALSb. One plant (RP6) was heterozygous for a Trp-574-Leu mutation on ALSa as well. Recombinant protein assays illustrate that the Ala-205-Phe mutation confers resistance to imidazolinone, sulfonylurea, triazolopyrimidines, sulfonylamino-carbonyl- triazolinones, and pyrimidinyl (thio) benzoate herbicides. In whole plant experiments, progeny with Ser-264-Gly or Ala-205-Phe mutations were controlled ≤ 11% by simazine or foramsulfuron compared to >98% for susceptible controls.

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