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dc.contributor.advisorBrowse, John A
dc.creatorHavko, Nathan Havko
dc.date.accessioned2017-06-19T16:22:01Z
dc.date.available2017-06-19T16:22:01Z
dc.date.issued2016
dc.identifier.urihttp://hdl.handle.net/2376/12028
dc.descriptionThesis (Ph.D.), Molecular Biosciences, Washington State Universityen_US
dc.description.abstractJasmonic acid (JA) is a plant hormone that controls many aspects of growth, development, and defense. As a defense hormone JA is rapidly synthesized in response to wounding, or attack from herbivores and pathogens, triggering the deployment of defense compounds. The activation of defenses by JA is accompanied by a potent repression of growth. This effect is thought to involve the diversion of resources from growth to defense. In this dissertation I investigated mechanisms regulating the plant wound response. In particular I performed genetic and biochemical studies on the JA-biosynthesis enzyme OPR3, which is implicated in the control of wound-induced JA biosynthesis. I found that OPR3 is chemically altered in wounded plants, and de-phosphorylation of an active site tyrosine hypothesized to control OPR3 activity is not necessary for OPR3 control in vivo. I also addressed the question of how JA signaling controls the balance between plant growth and defense. I performed a successful forward genetic screen to identify mutants that are insensitive to wound-induced growth inhibition. Seven mutants were identified which, unlike the wild-type, continue to grow during chronic wounding treatment. Four of these mutants maintain resistance to an insect herbivore and a necrotrophic pathogen suggesting that growth inhibition and the activation of defense responses can be uncoupled. I characterized one of the wound-insensitive mutants in detail. I show that the F-box protein, FBK51, is required for wound-induced growth inhibition, but not herbivore or pathogen resistance. I demonstrate that FBK51 interacts with the growth-promoting transcription factors VOZ1 and VOZ2, and the interaction leads to VOZ degradation. Transcriptional profiling of the wound response in fbk51 mutants suggests that a JA-independent pathway involving FBK51 may alter patterns of secondary metabolite accumulation and repression of photosynthesis. In summary, in this dissertation I address the question of how wounding triggers the rapid synthesis of JA, and how the wound response regulates the balance between plant growth and defense.en_US
dc.description.sponsorshipWashington State University, Molecular Biosciencesen_US
dc.language.isoEnglish
dc.rightsIn copyright
dc.rightsPublicly accessible
dc.rightsopenAccess
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/
dc.rights.urihttp://www.ndltd.org/standards/metadata
dc.rights.urihttp://purl.org/eprint/accessRights/OpenAccess
dc.subjectBiochemistryen_US
dc.subjectPlant sciencesen_US
dc.subjectFBK51en_US
dc.subjectJasmonateen_US
dc.subjectJasmonic aciden_US
dc.subjectOPR3en_US
dc.subjectPlant Defenseen_US
dc.titleJASMONATE BIOSYNTHESIS AND SIGNALING IN THE BALANCE OF PLANT GROWTH AND DEFENSE
dc.typeElectronic Thesis or Dissertation


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