期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2022
卷号：119
期号：9
DOI：10.1073/pnas.2105819119
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Significance
Synthetic auxin herbicides intersect basic plant developmental biology and applied weed management. We investigated resistance to 2,4-D in the Australian weed
Sisymbrium orientale (Indian hedge mustard). We identified a mechanism involving an in-frame 27-bp deletion in the degron tail of auxin coreceptor IAA2, one member of the gene family of Aux/IAA auxin co-receptors. We show that this deletion in IAA2 is a gain-of-function mutation that confers synthetic auxin resistance. This field-evolved mechanism of resistance to synthetic auxin herbicides confirms previous biochemical studies showing the role of the Aux/IAA degron tail in regulating Aux/IAA protein degradation upon auxin perception. The deletion mutation could be generated in crops using gene-editing approaches for cross-resistance to multiple synthetic auxin herbicides.
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 2,4-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 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.
