An in-frame deletion mutation in the degron tail of auxin coreceptor IAA2 confers resistance to the herbicide 2,4-D in Sisymbrium orientale

Marcelo R. A. de Figueiredo, Anita Kuepper, Jenna M. Malone, Tijana Petrovic, Ana Beatriz T. B. de Figueiredo, Grace Campagnola, Olve B. Peersen, Kasavajhala V. S. K. Prasad, Eric L. Patterson, Anireddy S. N. Reddy, Martin F. Kubes, Richard Napier, Franck E. Dayan, Christopher Preston, Todd A. Gaines

Research output: Contribution to journalArticlepeer-review

18 Citations (Scopus)

Abstract

The natural auxin indole-3-acetic acid (IAA) is a key regulator of many aspects of plant growth and development. Synthetic auxin herbicides such as 2,4-D mimic the effects of IAA by inducing strong auxinic-signaling responses in plants. 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 nine amino acids in the degron tail (DT) of the auxin coreceptor Aux/IAA2 (SoIAA2). The deletion allele cosegregated with 2,4-D resistance in recombinant inbred lines. Further, this deletion was also detected in several 2,4D-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 mechanism of synthetic auxin herbicide resistance assigns an in planta function to the DT region of this Aux/IAA coreceptor for its role in synthetic auxin binding kinetics and reveals a potential biotechnological approach to produce synthetic auxin-resistant crops using gene-editing.
Original languageEnglish
Article numbere2105819119
Number of pages9
JournalProceedings of the National Academy of Sciences of the United States of America
Volume119
Issue number9
DOIs
Publication statusPublished - 1 Mar 2022
Externally publishedYes

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