CORN POPPY (Papaver rhoeas) with GROUP B/2 resistance: (INHIBITION OF ACETOLACTATE SYNTHASE ) Inhibition of Acetolactate Synthase
MUTATION: TRYPTOPHAN 574 to LEUCINE
Corn Poppy (Papaver rhoeas) is a dicot plant in the papaveraceae family. A single amino acid substitution from Tryptophan 574 to Leucine has led to resistance to Inhibition of Acetolactate Synthase as indicated in the table below.		Corn Poppy

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

Délye, C., F. Pernin, And L. Scarabel.. 2011. Evolution and diversity of the mechanisms endowing resistance to herbicides inhibiting acetolactate-synthase (ALS) in corn poppy (Papaver rhoeas L.). Plant Science 180 : 333 - 342.

We investigated the diversity of mechanisms conferring resistance to herbicides inhibiting acetolactate synthase (ALS) in corn poppy (Papaver rhoeas L.) and the processes underlying the selection for resistance. Six mutant ALS alleles, Arg197, His197, Leu197, Ser197, Thr197 and Leu574 were identified in five Italian populations. Different alleles were found in a same population or a same plant. Comparison of individual plant phenotype (herbicide sensitivity) and genotype (amino-acid substitution(s) at codon 197) showed that all mutant ALS alleles conferred dominant resistance to the field rate of the sulfonylurea tribenuron and moderate or no resistance to the field rate of the triazolopyrimidine florasulam. Depending on the allele, dominant or partially dominant resistance to the field rate of the imidazolinone imazamox was observed. Putative non-target-site resistance mechanisms were also likely present in the populations investigated. The derived Cleaved Amplified Polymorphic Sequence assays targeting ALS codons crucial for herbicide sensitivity developed in this work will facilitate the detection of resistance due to mutant ALS alleles. Nucleotide variation around codon 197 indicated that mutant ALS alleles evolved by multiple, independent appearances. Resistance to ALS inhibitors in P. rhoeas clearly evolved by redundant evolution of a set of mutant ALS alleles and likely of non-target-site mechanisms.

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

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