Camelina mutants resistant to acetolactate synthase inhibitor herbicides

Abstract

Camelina (Camelina sativa L.) is a low-input oilseed crop of recent interest for sustainable biofuel production. As a relatively new crop in modern agriculture, considerable agronomic and regulatory problems need to be overcome. A common and troublesome problem is sensitivity to residues of acetolactate synthase (ALS) inhibitor herbicides in soils. To develop resistance to those residues, camelina seed were mutagenized by exposure to 0.3% ethyl methane sulfonate and screened at the M2 generation for increased resistance to imazethapyr and sulfosulfuron. Five lines with resistance were identified and characterized. Four mutants, identified in a screen for imazethapyr resistance (IM1, IM6, IM10, and IM18), appeared phenotypically identical and were controlled by the same co-dominant gene. One mutant identified in a screen for sulfosulfuron resistance was phenotypically different but also appears to be controlled by a single co-dominant gene. Further analysis with the IM1 and SM4 mutants confirmed they had increased resistance to imazethapyr, sulfosulfuron, and flucarbazone, with the resistance in the SM4 mutant being the highest. Compared to the wild type, doses of approximately 200 times more imazethapyr, 30 times more sulfosulfuron, and seven times as much flucarbazone were required to reduce plant growth by 50%. Sequence analysis of ALS genes from the SM4 line identified at least eight different genes or alleles. An allele associated with the highest levels of resistance was created by a single base substitution creating an amino acid shift previously found to cause ALS inhibitor resistance in yeast and tobacco.