Abstract
The multiple drug resistant mutant pdr1-1 was used to select for independent isolates with resistance to high levels of the herbicide sulfometuron methyl. Tetrad analyses of isolates identified a pdr1-1 gene interaction resulting in resistance to high levels of herbicide. All isolates were shown to carry new recessive mutations in the smr1 (ILV2) locus. Mutants of this locus also gave high herbicide resistance when combined with the smr3-21 mutation. However, pdr1-1 did not have an altered herbicide-resistance phenotype when combined with smr3-21 or a single gene suppressor (sur) of the pdr1-1 phenotype. It was suggested that the pdr1/smr1 interaction resulted from the additive effect of a cell permeability barrier and a resistant target enzyme (acetolactate synthase).