FLIXWEED (Descurainia sophia) with GROUP B/2 resistance: (INHIBITION OF ACETOLACTATE SYNTHASE ) Inhibition of Acetolactate Synthase
MUTATION: PROLINE 197 to LEUCINE
Flixweed (Descurainia sophia) is a dicot plant in the brassicaceae family. A single amino acid substitution from Proline 197 to Leucine has led to resistance to Inhibition of Acetolactate Synthase as indicated in the table below.		Flixweed

Chemical Family	Example Herbicide	Resistance Level
Imidazolinones	Imazethapyr	Not Determined
Pyrimidinyl benzoates	Bispyribac-Na	Not Determined
Sulfonylureas	Chlorsulfuron	Resistant > 10 fold
Triazolopyrimidine - Type 1	Chloransulam-methyl	Not Determined
Triazolinones	Flucarbazone-Na	Not Determined

REFERENCES

Cui HaiLan ; Zhang ChaoXian ; Wei ShouHui ; Zhang HongJun ; Li XiangJu ; Zhang YanQiu ; Wang GuiQi. 2011. Acetolactate synthase gene proline (197) mutations confer tribenuron-methyl resistance in flixweed (Descurainia sophia) populations from China. Weed Science 59 : 376 - 379.

The molecular basis of resistance to tribenuron-methyl, an acetolactate synthase (ALS) - inhibiting herbicide was investigated in four resistant (R) and three susceptible (S) flixweed populations. The resistance level in the R populations was assessed in whole-plant pot experiments in a greenhouse, and resistance indices ranged from 723 to 1422. The ALS genes of the three S populations and four R populations were cloned and sequenced, and the full coding sequence of the ALS gene of flixweed was 2,004 bp. The sequences of the ALS genes of the three S populations collected from Shaanxi, Gansu, and Tianjin were identical. Comparison of the ALS gene sequences of the S and R populations with Arabidopsis revealed that proline at position 197 of the ALS gene was substituted by leucine in R population SSX-2, by alanine in R population SSX-3, and by serine in R populations TJ-2 and GS-2. In another study of two R flixweed populations from Hebei and Shaanxi, resistance was also related to mutation at position 197 of the ALS gene. Both studies confirmed tribenuron-methyl resistance in flixweed in China, with the resistance mechanism being conferred by specific ALS point mutations at amino acid position 197..

Cui HaiLan ; Zhang ChaoXian ; Zhang HongJun ; Liu Xue ; Liu Yan ; Wang GuiQi ; Huang HongJuan ; Wei ShouHui. 2008. Confirmation of flixweed (Descurainia sophia) resistance to Tribenuron in China. Weed Science 56 : 775 - 779.

Reports arose from major Chinese wheat production regions that flixweed was not controlled by tribenuron after the herbicide was continuously used for several years. Flixweed seeds were collected from wheat fields that had been treated with tribenuron repeatedly over 3 to 15 yr or from road sides and remote hills that had never received tribenuron in Jiangsu, Hebei, Shanxi, Sichuan, Shandong, Shaanxi, and Henan provinces, and Tianjin and Beijing metropolises in China. The response of various biotypes to tribenuron was determined by whole plant experiments in the greenhouse. The experiments demonstrated that 11 of 32 flixweed biotypes were susceptible to tribenuron. The remaining 21 biotypes expressed moderate to high levels of tribenuron resistance with resistance indices ranging from 4 to >1,500. DNA sequence analysis of acetolactate synthase (ALS) genes of selected biotypes 6, 7, 27, and 29 revealed a point mutation at position 197 of the ALS gene, as numbered relative to the protein sequence of Arabidopsis, where proline was substituted by leucine in biotype 7 and by threonine in biotype 29. These mutations are known to confer resistance to ALS-inhibiting herbicides and are responsible for the high resistance of these biotypes to tribenuron. The results also indicate that tribenuron resistance in flixweed is widespread in China and management programs to control these resistant populations are warranted..

This case was entered by Patrick Tranel Email: tranel@illinois.edu

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