Using the Bacterial Plant Pathogen Pseudomonas syringae pv. tomato as a Model to Study the Evolution and Mechanisms of Host Range and Virulence

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dc.contributor.authorYan, Shuangchunen
dc.contributor.committeechairVinatzer, Boris A.en
dc.contributor.committeememberSetubal, João C.en
dc.contributor.committeememberJelesko, John G.en
dc.contributor.committeememberZhang, Liqingen
dc.contributor.committeememberTyler, Brett M.en
dc.contributor.departmentPlant Pathology, Physiology, and Weed Scienceen
dc.date.accessioned2017-04-06T15:44:34Zen
dc.date.adate2011-01-12en
dc.date.available2017-04-06T15:44:34Zen
dc.date.issued2010-12-06en
dc.date.rdate2016-10-18en
dc.date.sdate2010-12-20en
dc.description.abstractMost plant pathogens are specialists where only few plant species are susceptible, while all other plants are resistant. Unraveling the mechanisms behind this can thus provide valuable information for breeding or engineering crops with durable disease resistance. A group of Pseudomonas syringae strains with different host ranges while still closely related were thus chosen for comparative study. We confirmed their close phylogenetic relationship. We found evidence supporting that these strains recombined during evolution. The Arabidopsis thaliana and tomato pathogen P. syringae pv. tomato (Pto) DC3000 was found to be an atypical tomato strain, distinct from the typical Pto strains commonly isolated in the field that do not cause disease in A. thaliana, such as Pto T1. Comparing A. thaliana defense responses to DC3000 and T1, we found that T1 is eliciting stronger responses than DC3000. T1 is likely lacking Type III effector genes necessary to suppress plant defense. To test this, we sequenced the genomes of strains that cause and do not cause disease in A. thaliana. Comparative genomics revealed candidate effector genes responsible for this host range difference. Effector genes conserved in strains pathogenic in A. thaliana were expressed in T1 to test whether they would allow T1 to growth better in A. thaliana. Surprisingly, most of them reduced T1 growth. One of the effectors, HopM1, was of particular interest because it is disrupted in typical Pto strains. Although HopM1 has known virulence function in A. thaliana, HopM1 reduced T1 growth in both A. thaliana and tomato. HopM1 also increased the number of bacterial specks but reduced their average size in tomato. Our data suggest that HopM1 can trigger defenses in these plants. Additionally, transgenic detritivore Pseudomonas fluorescens that can secrete HopM1 shows dramatically increased growth in planta. The importance of genetic background of the pathogen for the functions of individual effectors is discussed. T1 cannot be manipulated to become an A. thaliana pathogen by deleting or adding individual genes. We now have a list of genes that can be studied in the future for the molecular basis of host range determination.en
dc.description.degreePh. D.en
dc.identifier.otheretd-12202010-021153en
dc.identifier.sourceurlhttp://scholar.lib.vt.edu/theses/available/etd-12202010-021153/en
dc.identifier.urihttp://hdl.handle.net/10919/77293en
dc.language.isoen_USen
dc.publisherVirginia Techen
dc.rightsIn Copyrighten
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/en
dc.subjecthost-microbe interactionen
dc.subjectcalloseen
dc.subjectHopM1en
dc.subjectmicrobial genomicsen
dc.subjectpopulation geneticsen
dc.subjectmolecular evolutionen
dc.subjectArabidopsis thalianaen
dc.subjectPseudomonas syringaeen
dc.titleUsing the Bacterial Plant Pathogen Pseudomonas syringae pv. tomato as a Model to Study the Evolution and Mechanisms of Host Range and Virulenceen
dc.typeDissertationen
dc.type.dcmitypeTexten
thesis.degree.disciplinePlant Pathology, Physiology, and Weed Scienceen
thesis.degree.grantorVirginia Polytechnic Institute and State Universityen
thesis.degree.leveldoctoralen
thesis.degree.namePh. D.en

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