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HopBA1, a pathogen virulence factor, reveals tissue-specific immune responses within the Pseudomonas syringae pv. tomato–Nicotiana benthamiana pathosystem

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dc.contributor.authorTodd, Tyler Scott, author
dc.contributor.authorNishimura, Marc, advisor
dc.contributor.authorSloan, Dan, committee member
dc.contributor.authorRoberts, Robyn, committee member
dc.date.accessioned2024-09-09T20:51:19Z
dc.date.available2024-09-09T20:51:19Z
dc.date.issued2024
dc.description.abstractPlant pathogens represent a major threat to food security as they dramatically reduce crop yield, impact the expression of desirable traits, and reduce post-harvest longevity. To infect host plants, bacteria like Pseudomonas syringae pv. tomato DC3000 (Pst DC3000) utilize a type III secretion system to deliver virulence proteins (also known as effectors) into the host cytoplasm to suppress immunity. In response, plants have evolved intracellular immune receptors that perceive immunosuppression and reactivate immunity. Thus, a given pathogen effector can both suppress and activate immunity depending on the host genome. Dissecting the molecular mechanisms of plant pathogen effectors helps inform our understanding of both disease and resistance. The present work reveals an uncharacterized role for Pst DC3000 as an aggressive vascular pathogen, causing systemic infection in the model plant Nicotiana benthamiana (Nb). Further, it establishes that the bacterial effector HopBA1 inhibits movement through the vascular system, despite increasing pathogen persistence within the primary infection site in leaves. Simultaneously, HopBA1 was found to induce irreversible upward vertical bending (i.e., hyponasty) in the petioles of infiltrated leaves, a novel phenotype for a bacterial effector. LC-MS/MS and RNA-Seq revealed phytohormone alteration (notably, a reduction in auxin and jasmonic acid-related metabolites) and transcriptional reprogramming of both developmental and defense genes. HopBA1-dependent growth restriction was suppressed in Nb eds1 (ENHANCED DISEASE SUSCEPTIBILITY 1) mutant plants, which still undergo HopBA1-induced hyponasty. Together, these results suggest that (1) HopBA1 triggers tissue-specific immune responses and (2) hyponasty is due to HopBA1's virulence activity, rather than host immune activation. Thus, HopBA1 in combination with the model pathogen Pst DC3000 becomes an important tool to dissect the poorly understood area of vascular-specific immunity. Vascular pathogens are particularly devastating and difficult to manage in crop species owing to the pathogen's internal location and systemic route of infection, making this research useful in crop improvement.
dc.format.mediumborn digital
dc.format.mediummasters theses
dc.identifierTodd_colostate_0053N_18582.pdf
dc.identifier.urihttps://hdl.handle.net/10217/239190
dc.languageEnglish
dc.language.isoeng
dc.publisherColorado State University. Libraries
dc.relation.ispartof2020-
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.subjectNicotiana benthamiana
dc.subjectplant-pathogen interactions
dc.subjectvascular immunity
dc.subjectplant pathology
dc.subjecteffector-triggered immunity
dc.subjectPseudomonas syringae
dc.titleHopBA1, a pathogen virulence factor, reveals tissue-specific immune responses within the Pseudomonas syringae pv. tomato–Nicotiana benthamiana pathosystem
dc.typeText
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.disciplineCell and Molecular Biology
thesis.degree.grantorColorado State University
thesis.degree.levelMasters
thesis.degree.nameMaster of Science (M.S.)

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