Biology subjects

Dayan, F. E.

Publications and source records attributed to Dayan, F. E..

3 recordsLinked to original sources

bioRxiv2024

A transposable element insertion in IAA16 interrupts normal splicing and generates a novel dicamba resistance allele in Bassia scoparia

A dicamba-resistant population of kochia (Bassia scoparia) identified in Colorado, USA in 2012 was used to generate a synthetic mapping population that segregated for dicamba resistance. Linkage mapping associating dicamba injury with genotype derived from restriction-site-associated DNA sequencing identified a single locus in the kochia genome associated with resistance on chromosome 4. A mutant version of Auxin/Indole-3-Acetic Acid 16 (AUX/IAA16; a gene previously implicated in dicamba resistance in kochia) was found near the middle of this locus in resistant plants. Long read sequencing of dicamba-resistant plants identified a recently inserted Ty1/Copia retrotransposon near the beginning of the second exon of AUX/IAA16, leading to disruption of normal splicing. A molecular marker for this insertion allows for rapid detection of resistance. Stable transgenic lines of Arabidopsis thaliana ectopically expressing the mutant and wildtype alleles of AUX/IAA16 were developed. Arabidopsis thaliana plants expressing the mutant AUX/IAA16 allele grew shorter roots on control media. However, transgenic root growth was less inhibited on media containing either dicamba (5 M) or IAA (0.5 M) when compared to non-transgenic plants or those expressing the wildtype allele of AUX/IAA16. In vitro assays indicate reduced binding affinity and more rapid dissociation of the mutant AUX/IAA with TIR1 in the presence of several auxins, and protein modeling suggests the substitution of the glycine residue in the degron domain of AUX/IAA16 is especially important for resistance. A fitness cost associated with the mutant allele of AUX/IAA16 has implications for resistance evolution and management of kochia populations with this resistance mechanism. SignificanceAuxin mimics 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 auxin perception and signalling. We describe a transposable element insertion within an herbicide target site gene that alters splicing and reduces synthetic and natural auxin perception.

plant biology↗

bioRxiv2023

CYTOCHROME P450 CYP72A219 IS INVOLVED IN EVOLUTION OF METABOLIC RESISTANCE TO TEMBOTRIONE IN Amaranthus palmeri POPULATIONS

Evolution of metabolic herbicide resistance is a major issue for weed management. Few genes and regulatory mechanisms have been identified, particularly in dicotyledonous weed species. We identified putative causal genes and regulatory mechanism for tembotrione-resistance in Amaranthus palmeri. Cytochrome P450 candidate genes were identified through RNA-seq analysis. We validated their functions using heterologous expression in S. cerevisae. Promoters of the candidate P450 genes were analyzed. We performed QTL mapping to identify genomic regions associated with resistance. CYP72A1182 deactivated tembotrione. This gene had increased expression in other A. palmeri populations resistant to multiple herbicides, including tembotrione. Resistant plants exhibited polymorphisms in the promoter of CYP72A1182. We identified QTLs linked to herbicide resistance, including one on chromosome 4 approximately 3 Mb away from CYP72A1182. CYP72A1182 is involved in tembotrione resistance in A. palmeri. Increased expression of this gene could be due to cis-regulation in the promoter, as well as trans-regulation from transcription factors. Further studies are in progress to test this hypothesis. The elucidation of regulatory genes is crucial for developing innovative weed management approaches and target-based novel molecules. HIGHLIGHTSOur study identifies that the CYP72A1182 gene has a functional role in metabolic herbicide resistance in Amaranthus palmeri and is linked to cis-regulatory polymorphisms, advancing metabolic resistance understanding in dicots.

plant biology↗

bioRxiv2023

Enhanced metabolic detoxification is associated with fluroxypyr resistance in Bassia scoparia

Auxin-mimic herbicides chemically mimic the phytohormone indole-3-acetic-acid (IAA). Within the auxin-mimic herbicide class, the herbicide fluroxypyr has been extensively used to control an agronomically problematic Great Plains tumbleweed, kochia (Bassia scoparia). A 2014 field survey for herbicide resistance in kochia populations across Colorado identified a putative fluroxypyr resistant population that was assessed for response to five different herbicides representing four different herbicide modes of action. These included fluroxypyr and dicamba (auxin-mimics), atrazine (photosystem II inhibitor), glyphosate (EPSPS inhibitor), and chlorsulfuron (acetolactate synthase inhibitor). The greenhouse screen identified that this kochia population was resistant to fluroxypyr and chlorsulfuron, but sensitive to glyphosate, atrazine, and dicamba. This population was designated Flur-R. Subsequent dose response studies determined that 75% of the Flur-R population survived 628 g ae ha-1 of fluroxypyr (4X the label application rate in wheat fallow, which is 157 g ae ha-1 at 1X). Flur-R was 40 times more resistant to fluroxypyr than a susceptible population (J01-S) collected from the same field survey (LD50 720 and 20 g ae ha-1, respectively). Auxin-responsive gene expression increased following fluroxypyr treatment in Flur-R, J01-S, and in a dicamba-resistant, fluroxypyr-susceptible line 9425 in an RNA-sequencing experiment. In Flur-R, several transcripts with molecular functions for conjugation and transport were constitutively higher expressed, such as glutathione S-transferases (GSTs), UDP-glucosyl transferase (GT), and ATP binding cassette transporters (ABC transporters). After analyzing metabolic profiles over time, both Flur-R and J01-S rapidly converted [14C]-fluroxypyr ester, the herbicide formulation applied to plants, to [14C]-fluroxypyr acid, the biologically active form of the herbicide, and three unknown metabolites. Formation and flux of these metabolites was faster in Flur-R than J01-S, reducing the concentration of phytotoxic fluroxypyr acid. One unique metabolite was present in Flur-R that was not present in the J01-S metabolic profile. Gene sequence variant analysis specifically for auxin receptor and signaling proteins revealed the absence of non-synonymous mutations affecting auxin signaling and binding in candidate auxin target site genes, further supporting our hypothesis that non-target site metabolic degradation is contributing to fluroxypyr resistance in Flur-R. Significance StatementHerbicide resistance is an ever-present issue in weeds of cropping and rangeland systems. By understanding genetic mechanisms of resistance in individual cases of herbicide resistance, we can extrapolate important information such as how quickly resistance to a specific herbicide can spread. Every characterized herbicide resistance mechanism contributes to a working database used to address herbicide resistance in an agricultural or open-space setting. Knowing the exact mechanism of resistance helps researchers and industry members understand why herbicide applications are failing, and if resistant plants can still be controlled with other herbicide modes of action. In kochia line Flur-R, there is strong evidence to support a non-target site resistance mechanism, specifically herbicide degradation via increased enzymatic activity. Increased fluroxypyr degradation represents a novel resistance mechanism to fluroxypyr in the weed Bassia scoparia.

plant biology↗