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BARLEY GRASS (Hordeum leporinum)
with GROUP B/2 resistance: (ALS INHIBITORS)
Inhibition of acetolactate synthase ALS (acetohydroxyacid synthase AHAS)

MUTATION: PROLINE 197 to SERINE

Barley Grass (Hordeum leporinum) 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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Barley Grass

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

NOTES

REFERENCES

Yu, Q., J. K. Nelson, M. Q. Zheng, M. Jackson, and S. B. Powles (2007). Molecular characterisation of resistance to ALS-inhibiting herbicides in Hordeum leporinum biotypes. Pest Management Science , 63 () : 918-927.

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.