BACKGROUND: Auxinic herbicides are widely used for selective control of many broadleaf weeds, e.g. wild mustard. An auxinic-herbicide-resistant wild mustard biotype may offer an excellent model system to elucidate the mechanism of action of these herbicides. Classical genetic analyses demonstrate that the wild mustard auxinic herbicide resistance is determined by a single dominant gene. Availability of near-isogenic lines (NILs) of wild mustard with auxinic herbicide resistance (R) and herbicide susceptibility (S) will help to study the fitness penalty as well as the precise characterization of this gene. RESULTS: Eight generations of backcrosses were performed, and homozygous auxinic-herbicide-resistant and auxinic-herbicide-susceptible NILs were identified from BC(8) F(3) families. S plants produced significantly more biomass and seed compared with R plants, suggesting that wild mustard auxinic herbicide resistance may result in fitness reduction. It was also found that the serrated margin of the first true leaf was closely linked to auxinic herbicide resistance. Using the introgressed progeny, molecular markers linked to auxinic herbicide resistance were identified, and a genetic map was constructed. CONCLUSION: The fitness penalty associated with the auxinic herbicide resistance gene may explain the relatively slow occurrence and spread of auxinic-herbicide-resistant weeds. The detection of the closely linked markers should hasten the identification and characterization of this gene.
BACKGROUND: Auxinic herbicides are widely used for selective control of many broadleaf weeds, e.g. wild mustard. An auxinic-herbicide-resistant wild mustard biotype may offer an excellent model system to elucidate the mechanism of action of these herbicides. Classical genetic analyses demonstrate that the wild mustard auxinic herbicide resistance is determined by a single dominant gene. Availability of near-isogenic lines (NILs) of wild mustard with auxinic herbicide resistance (R) and herbicide susceptibility (S) will help to study the fitness penalty as well as the precise characterization of this gene. RESULTS: Eight generations of backcrosses were performed, and homozygous auxinic-herbicide-resistant and auxinic-herbicide-susceptible NILs were identified from BC(8) F(3) families. S plants produced significantly more biomass and seed compared with R plants, suggesting that wild mustard auxinic herbicide resistance may result in fitness reduction. It was also found that the serrated margin of the first true leaf was closely linked to auxinic herbicide resistance. Using the introgressed progeny, molecular markers linked to auxinic herbicide resistance were identified, and a genetic map was constructed. CONCLUSION: The fitness penalty associated with the auxinic herbicide resistance gene may explain the relatively slow occurrence and spread of auxinic-herbicide-resistant weeds. The detection of the closely linked markers should hasten the identification and characterization of this gene.