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Multiple cases of ALS inhibitor-resistant weed biotypes are reported for many species, including wild mustard. The physiological extent and molecular basis of resistance to ALS inhibitors was compared in four biotypes of wild mustard from western Canada: a sulfonylurea (SU)-resistant (R) biotype from Manitoba detected in 1992; an SU (ethametsulfuron)-R biotype from Alberta detected in 1993 (metabolism-based resistance); an SU-R biotype from Manitoba detected in 2002; and a SU- and imidazolinone (IMI)-R biotype from Saskatchewan detected in 2002. Herbicide dose-response experiments confirmed that the two Manitoba biotypes were resistant to the SU herbicides ethametsulfuron and tribenuron : thifensulfuron mixture, whereas the Saskatchewan biotype was resistant to both SU herbicides and to imazethapyr, an IMI herbicide. Sequence analysis of the ALS gene detected target site mutations in three of the four R biotypes, with amino acid substitutions Pro 197 ( C CT) to Ser ( T CT) [Domain A of the gene] in the two SU-R Manitoba biotypes and Trp 574 (T G G) to Leu (T T G) [Domain B] in the Saskatchewan biotype. The Alberta SU-R biotype had the same ALS nucleotide and amino acid sequence as the susceptible population at these two positions. Two heterozygous individuals [Trp 574 (T t/g G)] were detected in the Saskatchewan biotype, and genetic segregation for nucleotide bases and resistance phenotype was consistent with single gene control. Nucleotide variation in neutral regions of the ALS gene varied with biotype, with no variation in the two Manitoba biotypes, two variants in the Saskatchewan biotype, and 16 neutral nucleotide polymorphisms (0.9%) in the Alberta biotype. The occurrence of at least three different ALS inhibitor-R biotypes in this important weed species is likely to impact negatively on the use of ALS inhibitors, such as the IMIs, and serves as a warning for strict implementation of herbicide rotations to prevent or delay the evolution and spread of such populations.