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Herbicide Resistance: Mechanisms, Inheritance, and Molecular Genetics

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Cross-resistance and Multiple-resistance

Often weeds will have resistance to more than one herbicide. Those herbicides may or may not be in related chemical families.

Plants with cross-resistance possess one mechanism that provides the ability to withstand herbicides from different chemical families. For example, a single point mutation in the enzyme acetolactate synthase (ALS) may provide resistance to the sulfonylurea and imidazolinone herbicide families. There are many different mutations and amino acid substitutions that can endow a plant with resistance to more than one family of ALS inhibitor herbicides.

Plants with multiple-resistance possess more than one mechanism that provides plants the ability to withstand herbicides from different chemical families. In this case, herbicide options become very limited. A Kochia scoparia population was identified that was target-site resistance to the PS II inhibitor herbicide, triazine, and to ALS inhibitor herbicides. The plants carried two mutations, one for resistance to each class of herbicide.

Weed populations also may have multiple herbicide-resistance mechanisms. For example, a Lolium rigidum population in Australia has target-site resistance to ACCase and to ALS inhibiting herbicides. In addition, it has metabolism-based resistance to a number of other herbicides from different chemical classes. There is evidence that different cytochrome P450s are responsible for the increased metabolism.


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