A transposable element insertion inIAA16interrupts normal splicing and generates a novel dicamba resistance allele inBassia scoparia

Abstract

SummaryA dicamba-resistant population of kochia (Bassia scoparia) previously identified in Colorado, USA in 2012 was used to generate a synthetic mapping population that segregated simply for dicamba resistance. Linkage mapping to associate injury following dicamba application with genotype information from restriction-site-associated DNA sequencing identified a single locus in the kochia genome associated with resistance on chromosome 4. A mutant version ofAuxin/Indole-3-Acetic Acid 16(AUX/IAA16; a gene previously implicated in dicamba resistance in kochia) is found near the middle of this locus in resistant plants. Long read sequencing of resistant plants identified a recently inserted Ty1/Copia retrotransposon near the beginning of exon two ofAUX/IAA16, leading to interruption of normal splicing. Stable transgenic lines ofArabidopsis thalianaectopically expressing the mutant and wildtype alleles ofAUX/IAA16were developed.Arabidopsis thalianaplants expressing the mutantAUX/IAA16allele grew shorter roots on control media but had less reduction in root growth on media containing either dicamba (5 μM) or IAA (0.5 μM) compared to non-transgenic plants or those expressing the wildtype allele ofAUX/IAA16.Protein modeling suggests the substitution of a specific glycine residue in the degron domain of AUX/IAA16 is especially important for resistance. A fitness cost associated with the mutant allele ofAUX/IAA16has implications for resistance evolution and management of kochia populations with this resistance mechanism. We report a molecular assay for rapid detection of the mutantAUX/IAA16allele that can inform in-season management decisions of agricultural producers.SignificanceSynthetic auxin herbicides are amongst the most important herbicides in modern agriculture. Evolution of weeds that are resistant to these herbicides threatens sustainable crop production. Understanding the basis of auxin herbicide resistance informs the development of improved weed control technologies. Additionally, auxin-resistant mutations and their pleotropic effects help us understand the role and function of natural and synthetic auxins. Here, we present the first report of a transposable element insertion within an herbicide target site gene leading to resistance and show that differential splicing leads to an adaptive allele. Our report advances the fields of auxin biology, weed management, and genome evolution.