The resistance of four populations of slender foxtail from England to chlorotoluron, pendimethalin, and the methyl ester of diclofop was studied in whole-plant spray assays. Two populations showed cross-resistance to all three herbicides while a third showed resistance to chlorotoluron only. Resistance, although not absolute, was sufficient to cause substantial reductions in herbicide performance at recommended field doses. Resistant (Peldon) and susceptible (Rothamsted) populations also were assessed for resistance to six dinitroaniline herbicides in a petri dish test in which the effects on shoot development were measured. The degree of resistance of the Peldon population varied considerably among herbicides, with greatest resistance to pendimethalin, whereas sensitivity to ethalfluralin, isopropalin, and trifluralin was similar to that of the Rothamsted standard. Differential response to butralin and oryzalin was smaller than to pendimethalin. The large difference between populations in their response to pendimethalin and trifluralin was confirmed in a pot experiment.

Herbicide-resistant weeds are a constraint to weed management in many cropping regions around the world. Of the numerous populations of weeds with resistance to herbicides, it appears that most have resistance due to an alteration to the target enzyme. Use of herbicides with alternative modes of action has relatively easily controlled these populations. In stark contrast are a much smaller number of populations with resistance due to increased rates of herbicide detoxification. These populations may be cross-resistant to herbicides with other modes of action. Such cross-resistance can severely compromise weed control because alternative herbicides may fail on their first use. It has proved extremely difficult to predict cross-resistance due to increased herbicide detoxification in weed populations and hence, difficult to provide adequate advice to growers on how to avoid or manage the problem. Most commonly, such cross-resistance has been selected by certain aryloxyphenoxypropanoate herbicides such as diclofop-methyl and phenylurea herbicides such as chlorotoluron and isoproturon; however, other herbicides can also act as selecting agents for this type of resistance. Illustrative examples from rigid ryegrass in Australia and blackgrass in Europe demonstrate the breadth of the problem and the magnitude of the effort required to understand increased herbicide detoxification as a resistance mechanism. Recent work has elucidated the genetic basis of cross-resistance in some populations, but this has so far not provided new predictive tools useful to growers. Despite more than a decade of research aimed at unraveling the complexities of cross-resistance due to increased herbicide detoxification, management of these cross-resistant populations remains a significant challenge.

The inheritance and linkage of enhanced metabolism-based herbicide cross-resistance was examined in a multiple resistant population of rigid ryegrass. F1 hybrids between resistant and susceptible populations showed an intermediate response to all the four herbicides tested, with no indication of maternal inheritance. Segregation of F2 families fitted a single-gene model for resistance to simazine, chlorotoluron, and chlorsulfuron. But there was more than the expected mortality from the low dose of tralkoxydim. Segregating F2 populations were selected by high rates of each of the four herbicides to create selected F2 families. Analysis of the response of these families demonstrated that simazine resistance is linked to chlorotoluron resistance. No other herbicide resistances were linked. Therefore, in this population of rigid ryegrass, at least three separate genes are responsible for metabolism-based cross-resistance. This study shows that multiple herbicide resistance in rigid ryegrass is the result of accumulation of a number of different resistance genes.