Mithila et al.: Inheritance of herbicide resistance • 417 Weed Science, 53:417–423. 2005 Inheritance of picloram and 2,4-D resistance in wild mustard (Brassica kaber) Mithila Jugulam Michael D. McLean Department of Environmental Biology, University of Guelph, Guelph, ON N1G 2W1, Canada J. Christopher Hall Corresponding author. Department of Environmental Biology, University of Guelph, Guelph, ON N1G 2W1, Canada; jchall@uoguelph.ca The primary goal of this research was to determine the inheritance of cross-resistance to several groups of auxinic herbicides through classical genetic approaches using auxinic herbicide–resistant (R) and –susceptible (S) wild mustard biotypes obtained from western Canada. F1 progeny were raised from crosses between homozygous auxinic herbicide–R and –S wild mustard parental lines. The F1 and F2 populations were assessed for picloram (pyridine group) and 2,4-D (phenoxyalkanoic group) resistance or susceptibility. Analyses of the F1 as well as the F2 progeny indicate that a single dominant gene confers the resistance to picloram and 2,4-D similar to an earlier report of dicamba-based (benzoic acid group) resistance in this wild mustard biotype. Furthermore, analyses of backcross progeny in this species indicate that resistance to all three auxinic herbicides, i.e., picloram, dicamba, and 2,4-D, is de- termined by closely linked genetic loci. With this information on inheritance of resistance to several auxinic herbicide families, the R biotype of wild mustard offers an excellent system to isolate and characterize the auxinic herbicide–resistance gene. Nomenclature: 2,4-D; picloram; wild mustard, Brassica kaber (DC) L.C. Wheeler SINAR. Key words: Auxinic herbicides, herbicide resistance, inheritance, near-isogenic lines. Herbicide resistance in plants is an inherited ability to survive and reproduce after exposure to a dose of herbicide normally lethal to the wild type. Cross-resistance refers to the expression of a mechanism that endows the ability to withstand herbicides from different chemical classes (having a similar mode of action) conferred by a single gene or, in the case of quantitative inheritance, by two or more genes (Hall et al. 1994). On the other hand, multiple cross-resis- tance refers to the inheritance of resistance to various classes of herbicides because of the action of multiple genes (Peever and Milgroom 1995). Resistance to herbicides results from repeated selection of resistant individuals in field popula- tions, and the resistant plants slowly increase in frequency in the presence of continued herbicide application (Devine and Shukla 2000). A plant is resistant to herbicides either because of differential absorption, translocation, metabo- lism, sequestration or because of altered target site. Prolonged use of herbicides has resulted in the develop- ment of resistance to several classes of herbicides including the auxinic herbicides, which have been in use for more than 60 yr. However, the incidence of auxinic herbicide resistance is low compared with other herbicide families such as the imidazolinones, sulfonylureas, and triazines because it has been reported in only 23 weed biotypes (Heap 2003). Fur- thermore, there is no widespread resistance to auxinic her- bicides. The rarity of auxinic herbicide resistance has been suggested to be because of their putative multiple sites of action (Gressel and Segel 1982), but this hypothesis has not been tested. On the basis of their structural and chemical properties, auxinic herbicides have been classified into several groups, viz., phenoxyalkanoic acids (e.g., 2,4-D, MCPA), benzoic acids (e.g., dicamba, chloramben), pyridines (e.g., picloram, clopyralid), and quinolinecarboxylic acids (e.g., quinclorac, quinmerac). Although there are structural differences among the various groups of auxinic herbicides, all these com- pounds cause similar physiological responses in sensitive spe- cies such as cell elongation, epinasty, hypertrophy, and ex- cessive ethylene biosynthesis (Sterling and Hall 1997). To elucidate the mechanism of auxinic herbicide resis- tance in wild mustard, resistant (R) and susceptible (S) bio- types (collected from Gilbert Plains and Minto Manitoba, Canada, respectively) have been extensively characterized at the morphological, physiological, and biochemical level (De- breuil et al. 1996; Peniuk et al. 1993; Webb and Hall 1995). Herbicide dose–response experiments indicate that the R biotype is 104, 18, and 10 times more resistant to picloram, 2,4-D and MCPA, respectively, than the S biotype (De- breuil et al. 1996; Heap and Morrison 1992). Subsequent investigations demonstrated that auxinic herbicide resistance is not due to differential absorption, translocation, or me- tabolism in this species (Peniuk et al. 1993). However, a possible role of altered target site in auxinic herbicide–in- duced responses has been suggested in R wild mustard (Webb and Hall 1995). Furthermore, inheritance of dicam- ba resistance in wild mustard (biotypes from Manitoba, Canada) was shown to be due to a single dominant nuclear gene (Jasieniuk et al. 1995). These data support the hy- pothesis of altered target site–induced auxinic herbicide re- sistance in wild mustard because it is believed that a single altered target site may result from single gene mutations (Darmency 1994). Thus, all these investigations (Jasieniuk et al. 1995; Webb and Hall 1995) provide evidence for po- tential occurrence of a mutation at a putative auxinic her- bicide site of action leading to resistance to these com- pounds in wild mustard. Although the physiological and biochemical effects of sev- eral auxinic herbicides belonging to different structural