A novel mutation in IAA16 is associated with dicamba resistance in Chenopodium album

Abstract

BACKGROUNDResistance to dicamba in Chenopodium album was first documented over a decade ago, however, the molecular basis of dicamba resistance in this species has not been elucidated. In this research, the resistance mechanism in a dicamba‐resistant C. album phenotype was investigated using a transcriptomics (RNA‐Seq) approach.RESULTSThe dose–response assay showed that the resistant phenotype (R) was nearly 25‐fold more resistant to dicamba than a susceptible phenotype (S) of C. album. Also, dicamba treatment significantly induced transcription of the known auxin‐responsive genes, Gretchen Hagen 3 (GH3), small auxin‐up RNAs (SAURs), and 1‐aminocyclopropane‐1‐carboxylate synthase (ACS) genes in the susceptible phenotype. Comparing the transcripts of auxin TIR/AFB receptors and AUX/IAA proteins identified from C. album transcriptomic analysis revealed that the R phenotype contained a novel mutation at the first codon of the GWPPV degron motif of IAA16, resulting in an amino acid substitution of glycine (G) with aspartic acid (D). Sequencing the IAA16 gene in other R and S individuals further confirmed that all the R individuals contained the mutation.CONCLUSIONIn this research, we describe the dicamba resistance mechanism in the only case of dicamba‐resistant C. album reported to date. Prior work has shown that the dicamba resistance allele confers significant growth defects to the R phenotype investigated here, suggesting that dicamba‐resistant C. album carrying this novel mutation in the IAA16 gene may not persist at high frequencies upon removal of dicamba application.

A transposable element insertion inIAA16disrupts splicing and causes dicamba resistance inBassia scoparia

“…LeClere et al (2018) showed that a substitution of this glycine to asparagine in BsAUX/IAA16 is sufficient for dicamba resistance in kochia. Similarly, Ghanizadeh et al (2024) associate a substitution of this glycine to aspartic acid with dicamba resistance in Chenopodium album, a closely related species. Finally, NMR experiments by Ramans-Harborough et al (2023) show that this glycine is involved in the interaction between IAA and TIR1.…”

“…A genome scan associating this genotype information to visual injury rating identified one significant QTL that peaks at 88 Mbp on chromosome 4 (Figure 2A). This interval contains BsAUX/IAA16 at 87.4 Mbp, a gene that is important for the signaling of auxin and has been implicated in auxin herbicide resistance in kochia and a closely related species (LeClere et al, 2018;Ghanizadeh et al, 2024). The genotype of BsAUX/IAA16 within this QTL of plants from an independent segregating F3 line explained 43% of variation in visual injury following dicamba treatment at 560 g ha -1 (Figure 2B).…”

“…Interestingly, all but one of these reports that specify a specific genetic basis (de Figueiredo et al, 2022a) pertain to mutations in or near the degron domain of Aux/IAA genes. LeClere et al (2018) and Ghanizadeh et al (2024) report, in closely related species, different mutations of a specific glycine residue in AUX/IAA16 that is known to be vital to normal auxin signaling. In an unrelated species, de Figueiredo et al (2022b) report a 27-bp deletion that shortens the distance between the degron and PB1 domains of IAA2.…”