Physiological and molecular characterization of mutation-derived imidazolinone resistance in spring wheat

While imidazolinone herbicides are an attractive alternative for weed control, spring wheat (Triticum aestivum L.) is susceptible to most of these herbicides. Three mutant alleles conferring resistance to the imidazolinone herbicides were previously identified in spring wheat following seed mutagenesis, hut little is known about the physiological and molecular basis of resistance conferred by these alleles. On the basis of acetohydroxyacid synthase (AHAS; E.C. 4.1.3.18) assays, imazethapyr resistance in genotypes TealIMI 10A (AhasL-D1), TealIMI 11A (AhasL-B1), TealIMI 15A, and BW755 (AhasL-D1) was due to a herbicide resistant form of AHAS. TealIMl 15A, which is homozygous for two resistance alleles, was the most resistant at the enzyme level, suggesting resistance in wheat is additive. Nucleotide sequence analysis of clones derived from susceptible cultivar CDC Teal and resistant lines indicated the presence of three genes coding for the catalytic subunit of AHAS. Using a collection of T. aestivum cv. Chinese Spring aneuploid and deletion lines, ahasL-D1, ahasL-B1, and ahasL-A1 mapped to the long arm of chromosomes 6D, 613, and 6A, respectively. Comparison of partial AhasL-D1, and AhasL-B1 deduced amino acid allele sequences with wild-type sequences indicated resistance was due to a Ser-Asn substitution near the carboxyl terminal of resulting AHAS catalytic subunits. This substitution was not present on the single isolated clone of AhasL-A1 from TealIMI 15A. This is the first report of the molecular characterization of the AHAS gene family from wheat.