The natural auxin indole-3-acetic acid (IAA) is a key regulator of many aspects of plant growth and development. Synthetic auxin herbicides mimic the effects of IAA by inducing strong auxinic signaling responses in plants. Synthetic auxins are crucial herbicides in agriculture, made more important by the recent introduction of transgenic synthetic auxin resistant soybean and cotton. Currently, 41 weed species have evolved resistance to synthetic auxin herbicides and, in all but one case, the molecular basis of these resistance mechanisms is unknown. To determine the mechanism of 2,4-D resistance in a Sisymbrium orientale (Indian hedge mustard) weed population, we performed a transcriptome analysis of 2,4-D-resistant (R) and -susceptible (S) genotypes that revealed an in-frame 27-nucleotide deletion removing 9 amino acids in the degron tail (DT) of the auxin co-receptor Aux/IAA2 (SoIAA2). The deletion allele co-segregated with 2,4-D resistance in recombinant inbred lines. Further, this deletion was also detected in several 2,4-D resistant field populations of this species. Arabidopsis transgenic lines expressing the SoIAA2 mutant allele were resistant to 2,4-D and dicamba. The IAA2-DT deletion reduced binding to TIR1 in vitro with both natural and synthetic auxins, causing reduced association and increased dissociation rates. This novel mechanism of synthetic auxin herbicide resistance assigns a new in planta function to the DT region of this Aux/IAA co-receptor for its role in synthetic auxin binding kinetics and reveals a potential biotechnological approach to produce synthetic auxin resistant crops using gene editing.
An in-frame deletion mutation in the degron tail of auxin co-receptor IAA2 confers resistance to the herbicide 2,4-D in Sisymbrium orientale
