Target‐site resistance and cross‐resistance to ALS‐inhibiting herbicides in radish and wild radish biotypes from Brazil

Abstract

AbstractRadish (Raphanus sativus L.) and wild radish (R. raphanistrum L.) are troublesome agricultural weeds in several areas worldwide, with populations resistant to acetolactate synthase (ALS) inhibitor herbicide. Information on the mechanisms of resistance is important for management and developing novel solutions to control resistant populations. The objective of this work was to determine the ALS‐resistance mechanisms in radish and wild radish biotypes resistant to ALS‐inhibiting herbicides. Resistance levels were determined by dose‐response curve using several rates of metsulfuron‐methyl herbicide in susceptible (JUC1) and resistant (JUC2, CRA3) radish, and susceptible (CAF1) and resistant (CAF2, CAF3) wild radish biotypes. The mechanism was evaluated by the in vitro activity of the ALS enzyme with imazapic herbicide and ALS gene sequencing. All resistant biotypes were insensitive to metsulfuron‐methyl and imazapic herbicides. The rate of metsulfuron‐methyl to reduce 50% growth of the plants (GR50) were 17‐ to 60‐fold (JUC2, CRA3) and 9‐ to 21‐fold (CAF2 and CAF3) higher than the susceptible biotypes of radish and wild radish, respectively. One‐point mutation in the ALS gene, Trp‐574‐Leu, was found in all resistant radish biotypes, whereas a second point mutation, Ala‐360‐Ser, was found in CAF2, CAF3, and JUC2 resistant biotypes. Changes in kinetic parameters of the ALS enzyme were found in all resistant biotypes evaluated, causing reduction of the herbicide affinity in the target‐site of action. Trp‐574‐Leu amino acid substitution resulted in resistance to sulfonylurea, imidazolinone, and triazolopyrimidine groups, with the survival greater than 75% of the plants, depending on the herbicide applied at labeled rate.