Herbicide Resistant Biotypes

Herbicide resistant weed populations have developed in several weed species. In some cases this is a result of a mutation which changed the physiological site at which the herbicide acts. This site-specific mutation results in a weed population resistant to a single herbicide or a group of herbicides with the same mode of action. Thus triazine resistant biotypes of dicotyledons have a photosynthetic pathway which has been altered by a specific mutation rendering it resistant to the standard triazine herbicides such as simazine and atrazine. An ACC-ase mutant Lolium rigidum weed population is resistant to the grass herbicides such as alloxydim and fluazifop which inhibit acetyl-coenzyme A carboxylase. An ALS mutant biotype of Lolium rigidum is resistant to the sulphonylurea and imidazolinone herbicides which inhibit acetolactate synthase.

Another type of resistance is a result of enhanced metabolism which may cause a range of herbicides with different modes of action to be more rapidly decomposed or deactivated by the resistant biotype than by the normal populations of the species. Thus certain biotypes of Lolium rigidum and Alopecurus myosuroides are weeds resistant to a wide range of herbicides such as chlortoluron, pendimethylin and dichlofop which are readily susceptible to metabolic breakdown.

A third mechanism which may be involved in development of resistance is exclusion of the toxin from the sites of physiological activity with which it interferes. This may involve reduced toxin uptake into the plant, reduced uptake into cells or partitioning into compartments of the cell where the toxin is less damaging. These mechanisms are thought to be involved in some cases of paraquat and heavy metal tolerance.

Note that more than one mechanism of resistance may be present in a single weed population, resulting in multiple resistance to a broad spectrum of herbicides, such as in several Australian populations of Lolium rigidum.

Return to table of resistant biotypes