INTERNATIONAL HERBICIDE-RESISTANT WEED DATABASE

MAYWEED CHAMOMILE (Anthemis cotula) with GROUP B/2 resistance: (INHIBITION OF ACETOLACTATE SYNTHASE ) Inhibition of Acetolactate Synthase

MUTATION: PROLINE 197 to LEUCINE

Mayweed Chamomile (Anthemis cotula) is a dicot plant in the asteraceae 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.		Mayweed Chamomile

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

NOTE

Different Pro197 substitutions were present within populations, and therefore specific cross resistance patterns conferred by specific substitutions are confounded.

REFERENCES

Intanon, S. ; Perez-Jones, A. ; Hulting, A. G. ; Mallory-Smith, C. A.. 2011. Multiple Pro₁₉₇ ALS substitutions endow resistance to ALS inhibitors within and among mayweed chamomile populations. Weed Science 59 : 431 - 437.

Mayweed chamomile seeds were collected from six different fields across the Pacific Northwest. All populations (each collection site was considered a population) were suspected to have some level of acetolactate synthase (ALS) resistance. Greenhouse and laboratory studies were conducted to determine if these populations were resistant to three different classes of ALS inhibitors: sulfonylureas (SU), imidazolinones (IMI), and triazolopyrimidines (TP). A whole-plant dose-response and in vitro ALS activity studies confirmed cross-resistance to thifensulfuron+tribenuron/chlorsulfuron (SU), imazethapyr (IMI), and cloransulam (TP); however, resistance varied by herbicide class and population. Two ALS isoforms of the ALS gene (ALS1 and ALS2) were identified in mayweed chamomile; however, only mutations in ALS1 were responsible for resistance. No mutations were found in ALS2. Sequence analysis of the partial ALS gene identified four point mutations at position 197 (Pro₁₉₇ to Leu, Gln, Thr, or Ser) in the resistant populations. This study demonstrates genotypic variation associated with cross-resistance to ALS inhibitors within and between populations..

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

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