COMMON SUNFLOWER (Helianthus annuus) with GROUP B/2 resistance: (INHIBITION OF ACETOLACTATE SYNTHASE ) Inhibition of Acetolactate Synthase
MUTATION: ALANINE 205 to VALINE
Common Sunflower (Helianthus annuus) is a dicot plant in the asteraceae family. A single amino acid substitution from Alanine 205 to Valine has led to resistance to Inhibition of Acetolactate Synthase as indicated in the table below.		Common Sunflower

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

REFERENCES

Kolkman, J. M. ; Slabaugh, M. B. ; Bruniard, J. M. ; Berry, S. ; Bushman, B. S. ; Olungu, C. ; Maes, N. ; Abratti, G. ; Zambelli, A. ; Miller, J. F. ; Leon, A. ; Knapp, S. J.. 2004. Acetohydroxyacid synthase mutations conferring resistance to imidazolinone or sulfonylurea herbicides in sunflower. Theoretical and Applied Genetics 109 : 1147 - 1159.

Wild biotypes of cultivated sunflower (Helianthus annuus L.) are weeds in corn (Zea mays L.), soybean (Glycine max L.), and other crops in North America, and are commonly controlled by applying acetohydroxyacid synthase (AHAS)-inhibiting herbicides. Biotypes resistant to two classes of AHAS-inhibiting herbicides - imidazolinones (IMIs) or sulfonylureas (SUs) - have been discovered in wild sunflower populations (ANN-PUR and ANN-KAN) treated with imazethapyr or chlorsulfuron, respectively. The goals of the present study were to isolate AHAS genes from sunflower, identify mutations in AHAS genes conferring herbicide resistance in ANN-PUR and ANN-KAN, and develop tools for marker-assisted selection (MAS) of herbicide resistance genes in sunflower. Three AHAS genes (AHAS1, AHAS2, and AHAS3) were identified, cloned, and sequenced from herbicide-resistant (mutant) and -susceptible (wild type) genotypes. We identified 48 single-nucleotide polymorphisms (SNPs) in AHAS1, a single six-base pair insertion-deletion in AHAS2, and a single SNP in AHAS3. No DNA polymorphisms were found in AHAS2 among elite inbred lines. AHAS1 from imazethapyr-resistant inbreds harbored a C-to-T mutation in codon 205 (Arabidopsis thaliana codon nomenclature), conferring resistance to IMI herbicides, whereas AHAS1 from chlorsulfuron-resistant inbreds harbored a C-to-T mutation in codon 197, conferring resistance to SU herbicides. SNP and single-strand conformational polymorphism markers for AHAS1, AHAS2, and AHAS3 were developed and genetically mapped. AHAS1, AHAS2, and AHAS3 mapped to linkage groups 2 (AHAS3), 6 (AHAS2), and 9 (AHAS1). The C/T SNP in codon 205 of AHAS1 cosegregated with a partially dominant gene for resistance to IMI herbicides in two mutant × wild-type populations. The molecular breeding tools described herein create the basis for rapidly identifying new mutations in AHAS and performing MAS for herbicide resistance genes in sunflower..

White, A. D. ; Graham, M. A. ; Owen, M. D. K.. 2003. Isolation of acetolactate synthase homologs in common sunflower. Weed Science 51 : 845 - 853.

A common sunflower population from Howard, SD (HSD) was previously determined to be cross-resistant to imazethapyr and chlorimuron-ethyl, both acetolactate synthase-inhibiting (ALS) herbicides. Experiments were conducted to determine if target-site polymorphisms could act as a mechanism of ALS-inhibitor herbicide resistance in the HSD common sunflower. Approximately 1600 nucleotides were amplified by polymerase chain reaction and sequenced from putative ALS gene(s) in common sunflower and Jerusalem artichoke. In sunflower, two different amplification products were detected that differed by a 9-basepair deletion. This suggested the presence of at least 2 ALS genes in common sunflower that could contribute to the herbicide resistance phenotype. In addition, an Ala₂₀₅ to Val₂₀₅ substitution was observed in several clones from resistant common sunflower (amino acid position is relative to the full-length mouse-ear cress ALS protein). Previously documented mutations at this position in other species indicated that it might play a vital role in conferring resistance to one or more ALS-inhibitor herbicides..

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

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