15.10 Herbicide Resistance to Seedling Shoot Growth Inhibitors

Resistance to the thiocarbamate herbicide triallate (Group 8) did not evolve until it had been used for more than 25 years.  Wild oat (Avena fatua) populations resistant to triallate were first documented in 1990 in Alberta and subsequently reported in Montana.  The resistant biotypes are unusual, because they represent metabolic loss-of-function mutants.  Thiocarbamate herbicides are actually pro-herbicides, in that they require metabolic activation by sulfoxidase enzymes to become phytotoxic.  In Montana, the resistant biotype was 10- to 15-fold slower at converting the triallate pro-herbicide into the phytotoxic triallate sulfoxide.  Both biotypes were equally susceptible to synthetic triallate sulfoxide, and the metabolism rates of this toxic form were equivalent.  Resistance was conferred by two recessive nuclear genes, which may encode the enzymes responsible for triallate sulfoxidation.  The mechanism of resistance in the Canadian biotype appears to involve alterations in gibberellin biosynthesis.  Interestingly, both biotypes are also cross-resistant to difenzoquat to  an unrelated pyrazolium herbicide that is no longer available for purchase.

This unusually long, resistance-free usage period illustrates several important concepts about plant responses to herbicide selection pressure.  First, even though triallate has a reasonably long soil half-life, its precise application requirements rarely allow it to achieve greater than about 85% wild oat control, and so it exerts less selection pressure compared to some other herbicides.  Second, the target species (wild oat) has relatively low seed production and poor seed dispersal, traits that tend to limit population sizes and thus reduce the frequency of potentially resistant individuals.  And third, the necessity of accumulating two separate recessive alleles to achieve resistance in self-pollinating wild oats would require a large number of individuals and generations.  If thiocarbamate herbicides in fact inhibit several elongases, the accumulation of additional alleles would require even more time.  It might be expected that the loss of two sulfoxidase-like activities would be associated with a fitness cost in the resistant biotype.  While fitness comparisons have not been done for the Montana biotypes, studies of the Canadian biotypes did not support this idea, and in fact seed germination was higher in the resistant lines.

Resistance to chloroacetamide herbicides (Group 15) has only been verified for barnyardgrass (China) and rigid ryegrass (Australia), and in both cases is based on enhanced metabolism.  The scarcity of resistant species is surprising, considering the long history and widespread use patterns of these herbicides.