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Physiological and biochemical mechanisms behind the fast action of glufosinate

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dc.contributor.authorKagueyama Takano, Hudson, author
dc.contributor.authorDayan, Franck E., advisor
dc.contributor.authorWestra, Philip, advisor
dc.contributor.authorReddy, Anireddy, committee member
dc.contributor.authorPreston, Christopher, committee member
dc.contributor.authorGaines, Todd, committee member
dc.date.accessioned2020-01-13T16:41:52Z
dc.date.available2021-01-07T16:41:53Z
dc.date.issued2019
dc.description.abstractGlufosinate is one of the few herbicides that are still effective for controlling herbicide resistant weeds, but its performance is often inconsistent and affected by environmental conditions. It inhibits glutamine synthetase (GS) by competing with glutamate for the active binding site. Unlike other amino acid biosynthesis inhibitors, glufosinate is a fast-acting herbicide and susceptible plants develop visual symptoms within a few hours after treatment. Inhibition of GS leads to ammonia accumulation and photosynthesis inhibition, which have traditionally been proposed as the causes of the rapid phytotoxicity. This dissertation presents a new understanding of the mechanism(s) of action of glufosinate and a biochemical approach to improve its herbicidal efficacy. Glufosinate uptake is inhibited by glutamine levels in the plant, and translocation is not affected by the rapid phytotoxicity. Glufosinate translocates primarily through the apoplast (xylem) rather than the symplast (phloem) probably due to its physicochemical properties and the absence of an effective membrane transporter. Glufosinate efficacy is proportional to the herbicide concentration in leaf tissues. Neither ammonia accumulation nor carbon assimilation inhibition are directly associated with the fast action of glufosinate. Instead, rapid phytotoxicity results from a massive light-dependent accumulation of reactive oxygen species (ROS). Inhibition of GS blocks the photorespiration pathway leading to a massive photooxidation damage. Under full sunlight, the excess of electrons is accepted by molecular oxygen leading to ROS generation. These free radicals cause lipid peroxidation, which ultimately leads to rapid cell death. The addition of protoporphyrinogen oxidase (PPO) inhibitors to glufosinate enhances ROS accumulation and herbicidal activity. This enhanced activity results from protoporphyrin formation at high levels due to a transient accumulation of glutamate, the precursor for chlorophyll biosynthesis. The herbicide combination also showed enhanced activity in the field and may help to overcome the lack of glufosinate efficacy under certain environmental conditions.
dc.format.mediumborn digital
dc.format.mediumdoctoral dissertations
dc.identifierKagueyamaTakano_colostate_0053A_15779.pdf
dc.identifier.urihttps://hdl.handle.net/10217/199807
dc.languageEnglish
dc.language.isoeng
dc.publisherColorado State University. Libraries
dc.relation.ispartof2000-2019
dc.rightsCopyright and other restrictions may apply. User is responsible for compliance with all applicable laws. For information about copyright law, please see https://libguides.colostate.edu/copyright.
dc.subjectherbicides
dc.subjectmode of action
dc.subjectreactive oxygen species
dc.subjectmetabolomics
dc.subjectglutamine synthetase
dc.subjectphosphinothricin
dc.titlePhysiological and biochemical mechanisms behind the fast action of glufosinate
dc.typeText
dcterms.embargo.expires2021-01-07
dcterms.embargo.terms2021-01-07
dcterms.rights.dplaThis Item is protected by copyright and/or related rights (https://rightsstatements.org/vocab/InC/1.0/). You are free to use this Item in any way that is permitted by the copyright and related rights legislation that applies to your use. For other uses you need to obtain permission from the rights-holder(s).
thesis.degree.disciplineBioagricultural Sciences and Pest Management
thesis.degree.grantorColorado State University
thesis.degree.levelDoctoral
thesis.degree.nameDoctor of Philosophy (Ph.D.)

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