Physiological Characterization of Picloram Resistance in Yellow Starthistle

Fuerst, E. Patrick; Sterling, Tracy M.; Norman, Michael; Prather, Timothy S.; Irzyk, Gerard P.; Wu, Yujia; Lownds, Norman K.; Callihan, R. H.

doi:10.1006/pest.1996.0069

Cited by 40 publications

(44 citation statements)

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“…However, an isolated occurrence of field resistance to picolinate auxins has been documented in yellow starthistle (Centaurea solstitialis) and appears to have arisen from heavy localized use of picloram. This resistant biotype carries a recessive mutation (Sabba et al, 2003) that confers selective resistance to picloram and clopyralid, but not to 2,4-D, and it also has normal growth and morphology (Fuerst et al, 1996). Thus, the picloramresistant field biotype appears to have some of the characteristics associated with the mutations that we have identified in Arabidopsis.…”

Section: Relevance To Herbicidal Auxin Resistance and Selectivity In mentioning

confidence: 75%

Mutations in an Auxin Receptor Homolog AFB5 and in SGT1b Confer Resistance to Synthetic Picolinate Auxins and Not to 2,4-Dichlorophenoxyacetic Acid or Indole-3-Acetic Acid in Arabidopsis

et al. 2006

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Although a wide range of structurally diverse small molecules can act as auxins, it is unclear whether all of these compounds act via the same mechanisms that have been characterized for 2,4-dichlorophenoxyacetic acid (2,4-D) and indole-3-acetic acid (IAA). To address this question, we used a novel member of the picolinate class of synthetic auxins that is structurally distinct from 2,4-D to screen for Arabidopsis (Arabidopsis thaliana) mutants that show chemically selective auxin resistance. We identified seven alleles at two distinct genetic loci that conferred significant resistance to picolinate auxins such as picloram, yet had minimal cross-resistance to 2,4-D or IAA. Double mutants had the same level and selectivity of resistance as single mutants. The sites of the mutations were identified by positional mapping as At4g11260 and At5g49980. At5g49980 is previously uncharacterized and encodes auxin signaling F-box protein 5, one of five homologs of TIR1 in the Arabidopsis genome. TIR1 is the recognition component of the Skp1-cullin-F-box complex associated with the ubiquitin-proteasome pathway involved in auxin signaling and has recently been shown to be a receptor for IAA and 2,4-D. At4g11260 encodes the tetratricopeptide protein SGT1b that has also been associated with Skp1-cullin-F-box-mediated ubiquitination in auxin signaling and other pathways. Complementation of mutant lines with their corresponding wild-type genes restored picolinate auxin sensitivity. These results show that chemical specificity in auxin signaling can be conferred by upstream components of the auxin response pathway. They also demonstrate the utility of genetic screens using structurally diverse chemistries to uncover novel pathway components.

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Section: Relevance To Herbicidal Auxin Resistance and Selectivity In mentioning

confidence: 75%

Mutations in an Auxin Receptor Homolog AFB5 and in SGT1b Confer Resistance to Synthetic Picolinate Auxins and Not to 2,4-Dichlorophenoxyacetic Acid or Indole-3-Acetic Acid in Arabidopsis

et al. 2006

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“…Herbicide resistance mechanisms have been categorized into two types, (a) non‐target‐site, involving decreased absorption, translocation and/or enhanced herbicide metabolism, and (b) target‐site, resulting from mutations in the target gene or increases in levels of the target protein through gene amplification or transcriptional upregulation . Previous research found that auxinic herbicide resistance in wild mustard ( Sinapis arvensis ), false cleavers ( Galium spurium ), kochia ( Kochia scoparia ), and yellow starthistle ( Centaurea solstitialis ) was not attributable to differences in herbicide absorption, translocation and/or metabolism and, by deduction, might be attributable to other mechanisms, such as altered target site. A different dicamba‐resistant K. scoparia population was found to have reduced dicamba translocation …”

Section: Discussionmentioning

confidence: 99%

Metabolism of 2,4‐dichlorophenoxyacetic acid contributes to resistance in a common waterhemp (Amaranthus tuberculatus) population

Figueiredo

Leibhart

Reicher

et al. 2018

Pest Management Science

109

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Figueiredo, Marcelo R. A.; Leibhart, Lacy J.; Reicher, Zachary J.; Tranel, Patrick J.; Nissen, Scott J.; Westra, Philip; Bernards, Mark L.; Kruger, Greg R.; Gaines, Todd A.; and Jugulam, Mithila, "Metabolism of 2,4-dichlorophenoxyacetic acid contributes to resistance in a common waterhemp (Amaranthus tuberculatus) population" (2017 This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi: 10.1002/ps.

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“…Picloram Picloram is a synthetic auxin (Fuersta et al, 1996) There was one case associated with use of picloram in the handler database that did not involve direct contact (see Table 28.6). The single case reported in the handler database indicated that occlusion of molinate against the skin inside protective clothing may cause dermal irritation (see Table 28.6).…”

Section: Pyridine Carboxylic Acidsmentioning

confidence: 99%

The Regulatory Evaluation of the Skin Effects of Pesticides

O’Malley

2010

Hayes' Handbook of Pesticide Toxicology

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Physiological Characterization of Picloram Resistance in Yellow Starthistle

Cited by 40 publications

References 0 publications

Mutations in an Auxin Receptor Homolog AFB5 and in SGT1b Confer Resistance to Synthetic Picolinate Auxins and Not to 2,4-Dichlorophenoxyacetic Acid or Indole-3-Acetic Acid in Arabidopsis

Mutations in an Auxin Receptor Homolog AFB5 and in SGT1b Confer Resistance to Synthetic Picolinate Auxins and Not to 2,4-Dichlorophenoxyacetic Acid or Indole-3-Acetic Acid in Arabidopsis

Metabolism of 2,4‐dichlorophenoxyacetic acid contributes to resistance in a common waterhemp (Amaranthus tuberculatus) population

The Regulatory Evaluation of the Skin Effects of Pesticides

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