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DOWNY BROME (Bromus tectorum)
with GROUP B/2 resistance: (ALS INHIBITORS)
Inhibition of acetolactate synthase ALS (acetohydroxyacid synthase AHAS)

MUTATION: PROLINE 197 to SERINE

Downy Brome (Bromus tectorum) is a monocot plant in the poaceae family. A single amino acid substitution from Proline 197 to Serine has led to resistance to ALS inhibitors as indicated in the table below.

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Downy Brome

Chemistry	Example	Resistance
Imidazolinones	Imazethapyr	Susceptible
Pyrimidinylthiobenzoates	Bispyribac-Na	Not Determined
Sulfonylureas	Chlorsulfuron	Resistant > 10 fold
Triazolopyrimidines	Chloransulam-methyl	Not Determined
Sulfonylaminocarbonyltriazolinone	Flucarbazone-Na	Resistant > 10 fold
Triazolinone	Amicarbazone	Not Determined

NOTES

REFERENCES

Park, K. W. and C. A. Mallory Smith (2004). Physiological and molecular basis for ALS inhibitor resistance in Bromus tectorum biotypes. Weed Research , 44 (2) : 71-77.

Primisulfuron-resistant (AR and MR) and -susceptible (AS and MS) Bromus tectorum biotypes were collected from a Poa pratensis field at Athena, Oregon, and in research plots at Madras, Oregon. Studies were conducted to characterize the resistance of the B. tectorum biotypes. Whole plant bioassay and acetolactate synthase (ALS) enzyme assay revealed that the AR biotype was highly resistant to the sulfonylurea (SU) herbicides, primisulfuron and sulfosulfuron and to a sulfonylaminocarbonyltriazolinone (SCT) herbicide, propoxycarbazone-sodium. However, the AR biotype was not resistant to imazamox, an imidazolinone (IMI) herbicide. Results of the whole plant bioassay studies showed that the MR biotype was moderately resistant to all ALS inhibitors tested. However, there were no differences in ALS sensitivities between the MR and MS biotypes. The nucleotide and amino acid sequence analysis of the als gene demonstrated a single-point mutation from C to T, conferring the exchange of the amino acid proline to serine at position 197 in the AR biotype. However, this mutation was not found in the MR biotype. Results of this research indicate that: the resistance of the AR biotype to SU and SCT herbicides is based on an altered target site due to a single-point mutation; resistance in the MR biotype is not due to a target site mutation.