An 18 base pair in-frame deletion in the degron tail of IAA2 provides resistance to 2,4-D and dicamba in Brassica tournefortii.

A population of Brassica tournefortii from South Australia was suspected to be resistant to 2,4-D. This study aimed to determine whether resistance to 2,4-D and other auxinic herbicides was present in the population and identify possible resistance mechanisms. The population was resistant (R) to 2,4-D, with an LD of 333 g ha, which is 8.4 times higher than the LD of the susceptible (S) population at 39.6 g ha. The R population was also cross-resistant to other auxin herbicides, including MCPA, dicamba, fluroxypyr, triclopyr, and picloram. When treated with 2,4-D plus malathion, the R population had an LD of 325 g ha, compared to 333 g ha when treated with 2,4-D alone, suggesting that metabolic detoxification was not involved in resistance to this herbicide. Molecular analysis revealed an in-frame deletion in the IAA2 gene of the R population, spanning the degron and degron tail regions, which are critical for auxin-induced degradation of Aux/IAA proteins. This deletion was not present in the S population, nor in four other S populations screened in this study. These findings indicate that the deletion is unique to the R population and likely contributes directly to the resistance phenotype. Overall, the results confirm that resistance to 2,4-D in this B. tournefortii population is due to a target-site mutation in IAA2, and that this mutation may also confer cross-resistance to other auxinic herbicides.