Isolation and Characterization of Tn5 Mutants of Pseudomonas Syringae Pv. Phaseolicola which Fail to Elicit a Hypersensitive Response

Deasey, Mary C.; Stapleton, Megan; Matthysse, Ann G.

doi:10.1007/978-94-009-3555-6_88

Cited by 3 publications

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References 6 publications

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“…(i) Several genes required for elicitation of the HR have been identified by Tn5 mutagenesis (5,6,16,23), and some have been cloned (14,19). These hrp genes are required for both the HR and pathogenicity and appear to be present in all P. syr-ingae pathovars (13,14,21).…”

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Molecular cloning of a Pseudomonas syringae pv. syringae gene cluster that enables Pseudomonas fluorescens to elicit the hypersensitive response in tobacco plants

et al. 1988

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A cosmid clone isolated from a genomic library of Pseudomonas syringae pv. syringae 61 restored to all Tn5 mutants of this strain studied the ability to elicit the hypersensitive response (HR) in tobacco. Cosmid pHIR11 also enabled Escherichia coli TB1 to elicit an HR-like reaction when high levels of inoculum (109 cells per ml)were infiltrated into tobacco leaves. The cosmid, which contains a 31-kilobase DNA insert, was mobilized by triparental matings into Pseudomonasfluorescens 55 (a nonpathogen that normally causes no plant reactions), P. syringae pv. syringae 226 (a tomato pathogen that causes the HR in tobacco), and P. syringae pv. tabaci (a tobacco pathogen that causes the HR in tomato). The plant reaction phenotypes of all of the transconjugants were altered. P. fluorescens(pHIR11) caused the HR in tobacco and tomato leaves and stimulated an apparent proton influx in suspension-cultured tobacco cells that was indistinguishable from the proton influx caused by incompatible pathogenic pseudomonads. P. syringae pv. tabaci(pHIR11) and P. syringae pv. syringae 226(pHIR11) elicited the HR rather than disease symptoms on their respective hosts and were no longer pathogenic. pHIR11 was mutagenized with TnphoA (TnS ISSOL::phoA). One randomly chosen mutant, pHIR11-18, no longer conferred the HR phenotype to P. fluorescens. The mutation was marler-exchanged into the genomes of P. syringae pv. syringae strains 61 and 226. The TnphoA insertions in the two pseudomonads abolished their ability to elicit any plant reactions in all plants tested. The results indicate that a relatively small portion of the P. syringae genome is sufficient for the elicitation of plant reactions.The hypersensitive response (HR) of higher plants is characterized by the rapid, localized necrosis of tissues invaded by an incompatible pathogen (a microorganism that is pathogenic only on another host) and is associated with resistance to the pathogen (11). Elicitation of the HR by phytopathogenic bacteria is readily observed by infiltrating leaves with suspensions containing >106 bacteria per ml (10). Tobacco leaf tissue collapses within 24 h after inoculation with Pseludomonas syringae pv. syringae, for example. (5,6,16,23), and some have been cloned (14,19). These hrp genes are required for both the HR and pathogenicity and appear to be present in all P. syr-ingae pathovars (13,14,21

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Molecular cloning of a Pseudomonas syringae pv. syringae gene cluster that enables Pseudomonas fluorescens to elicit the hypersensitive response in tobacco plants

et al. 1988

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“…syringae , Baker etal. 1987, Niepold et al 1985, Panopoulis et al 1985, tomato (Bender et al 1987, Cuppels, 1986, phaseolicola , Deasey et al 1987, Lindgren et al 1986, 1988Somlyai et al 1986), mdpisi (Malik et al 1987). In general, mutants were identified by their failure to produce symptoms on compatible hosts or HR in tobacco leaves.…”

Section: Current Insights Into the Genetic Basis For The Ability Of Pmentioning

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Elicitation of the hypersensitive response by Pseudomonas syringae

Hutcheson

Collmer

Baker

1989

Physiologia Plantarum

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1989. Elicitation of the hypersensitive response by Pseudomonas syringae. -Physiol. Plant. 76: 155-163.The hypersensitive response (HR), a rapid local necrosis accompanied by the production of antimicrobial compounds, is a manifestation of the primary defense mechanisms through which plants prevent colonization by potentially pathogenic microorganisms. The pathogen factors that trigger HR-associated defense mechanisms have yet to be established. Apphcation of transposon mutagenesis and molecular cloning techniques have provided new insights into the bacterial elicitation of the HR. This review focuses on the interaction of Pseudomonas syringae with non-host plants as a model system for the bacterial induction of the HR and discusses (a) the genetics of Pseudomonas syringae pathogenicity and HR elicitation, (b) the environmental conditions controlling expression of Pseudomonas syringae pathogenicity/HR determinants, (c) the nature of the HR elicitor and (d) early plant responses to the pathogen.

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Organization and Expression of the hrp Gene Cluster in Pseudomonas Syringae Pv. Phaseolicola

Rahme

Mindrinos

Grimm

et al. 1989

Vascular Wilt Diseases of Plants

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Isolation and Characterization of Tn5 Mutants of Pseudomonas Syringae Pv. Phaseolicola which Fail to Elicit a Hypersensitive Response

Cited by 3 publications

References 6 publications

Molecular cloning of a Pseudomonas syringae pv. syringae gene cluster that enables Pseudomonas fluorescens to elicit the hypersensitive response in tobacco plants

Molecular cloning of a Pseudomonas syringae pv. syringae gene cluster that enables Pseudomonas fluorescens to elicit the hypersensitive response in tobacco plants

Elicitation of the hypersensitive response by Pseudomonas syringae

Organization and Expression of the hrp Gene Cluster in Pseudomonas Syringae Pv. Phaseolicola

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