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Browsing Research Data - Other by Author "Gaines, Todd A."

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    Dataset associated with “An in-frame deletion mutation in the degron tail of auxin co-receptor IAA2 confers resistance to the herbicide 2,4-D in Sisymbrium orientale”
    (Colorado State University. Libraries, 2021) de Figueiredo, Marcelo R. A.; Küpper, Anita; Malone, Jenna M.; Petrovic, Tijana; de Figueiredo, Ana Beatriz T. B.; Campagnola, Grace; Peersen, Olve B.; Prasad, Kasavajhala V.S.K.; Patterson, Eric L.; Reddy, Anireddy S. N.; Kubeš, Martin F.; Napier, Richard; Dayan, Franck E.; Preston, Christopher; Gaines, Todd A.
    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 9 amino acids in the degron tail (DT) of the auxin co-receptor Aux/IAA2 (SoIAA2). The deletion allele co-segregated 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 novel mechanism of synthetic auxin herbicide resistance assigns a new in planta function to the DT region of this Aux/IAA co-receptor for its role in synthetic auxin binding kinetics and reveals a potential biotechnological approach to produce synthetic auxin resistant crops using gene editing.
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    ItemOpen Access
    Dataset associated with “Genomic‐based epidemiology reveals independent origins and gene flow of glyphosate resistance in Bassia scoparia populations across North America"
    (Colorado State University. Libraries, 2020) Ravet, Karl; Sparks, Crystal D.; Dixon, Andrea; Küpper, Anita; Westra, Eric P.; Pettinga, Dean J.; Tranel, Patrick J.; Felix, Joel; Morishita, Don W.; Jha, Prashant; Kniss, Andrew; Stahlman, Phillip W.; Neve, Paul; Patterson, Eric L.; Westra, Philip; Gaines, Todd A.
    Genomic-based epidemiology can provide insight into the origins and spread of herbicide resistance mechanisms in weeds. We used kochia (Bassia scoparia) populations resistant to the herbicide glyphosate from across western North America to test the alternative hypotheses that 1) a single EPSPS gene duplication event occurred initially in the Central Great Plains and then subsequently spread to all other geographical areas now exhibiting glyphosate-resistant kochia populations or that 2) gene duplication occurred multiple times in independent events in a case of parallel evolution. We used qPCR markers previously developed for measuring the structure of the EPSPS tandem duplication to investigate whether all glyphosate-resistant individuals had the same EPSPS repeat structure. We also investigated population structure using simple sequence repeat (SSR) markers to determine the relatedness of kochia populations from across the Central Great Plains, Northern Plains, and the Pacific Northwest. We found that the original EPSPS duplication genotype was predominant in the Central Great Plains where glyphosate resistance was first reported. We identified two additional EPSPS-duplication genotypes, one having geographic associations with the Northern Plains and the other to the Pacific Northwest. The EPSPS duplication genotype from the Pacific Northwest seems likely to represent a second, independent evolutionary origin of a resistance allele. We found evidence of gene flow across populations and a general lack of population structure. The results support at least two independent evolutionary origins of glyphosate resistance in kochia, followed by substantial and mostly geographically localized gene flow to spread the resistance alleles into diverse genetic backgrounds.