Todd, O. E. | bioRxiv Science

bioRxiv2024

A standard area diagram for Fusarium yellows rating in sugar beet (Beta vulgaris L.)

Members of the Fusarium oxysporum species complex are pathogens of sugar beet causing Fusarium yellows. Fusarium yellows can reduce plant stand, yield, and extractable sugar. Improving host plant resistance against Fusarium-induced diseases, like Fusarium yellows, represents an important long-term breeding target in sugar beet breeding programs. Current methods for rating Fusarium yellows disease severity rely on an ordinal scale, which limits precision for intermediate phenotypes. In this study, we aimed to improve the accuracy and precision of rating Fusarium yellows by developing a standard area diagram (SAD). Two SAD versions were created using images of sugar beets infected with Fusarium oxysporum strain F19. Each version was tested using inexperienced raters. Comparing both the pilot and improved version showed no statistical differences in Lins Concordance Correlation Coefficient (LCC) values to assess accuracy and precision between the two versions (Cb = 0.99 for both versions, {rho}c = 0.97 and 0.96 for version 1 and 2, respectively). In addition, five naive Bayesian machine learning models which used pixel classification to determine disease score, were tested for congruency to human estimates in version 2. Root mean square error was lowest compared to the "true" values for the unweighted model and a model where necrotic tissue was given a 2x weight (12.4 and 12.6, respectively). The creation of this standard area diagram enables breeding programs to make consistent, accurate disease ratings regardless of personnels previous experience with Fusarium yellows. Additionally, more iterations of pixel quantification equations may overcome accuracy issues for rating Fusarium yellows.

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↗