Layered basal defenses underlie non-host resistance of Arabidopsis to Pseudomonas syringae pv. phaseolicola

Authors

  • Jong Hyun Ham,

    1. Department of Horticulture and Crop Science, The Ohio State University,
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    • These authors contributed equally to this work.

  • Min Gab Kim,

    1. Department of Horticulture and Crop Science, The Ohio State University,
    2. Department of Plant Cellular and Molecular Biology, The Ohio State University,
    3. Program in Plant Molecular Biology and Biotechnology, Program in Molecular Cellular and Developmental Biology, Rm. 306C Kottman Hall, The Ohio State University, Columbus, OH 43210, USA
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    • These authors contributed equally to this work.

  • Sang Yeol Lee,

    1. Program in Plant Molecular Biology and Biotechnology, Program in Molecular Cellular and Developmental Biology, Rm. 306C Kottman Hall, The Ohio State University, Columbus, OH 43210, USA
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  • David Mackey

    Corresponding author
    1. Department of Horticulture and Crop Science, The Ohio State University,
    2. Department of Plant Cellular and Molecular Biology, The Ohio State University,
    3. Environmental Biotechnology National Core Research Center, Gyeongsang National University, Jinju 660-701, Korea, and
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(fax +614 292 7162; e-mail mackey.86@osu.edu).

Summary

Arabidopsis is a non-host for Pseudomonas syringae pv. phaseolicola NPS3121 (Pph), a bacterial pathogen of bean. Pph does not induce a hypersensitive response in Arabidopsis. Here we show that Arabidopsis instead resists Pph with multi-layered basal defense. Our approach was: (i) to identify defense readouts induced by Pph; (ii) to determine whether mutations in known Arabidopsis defense genes disrupt Pph-induced defense signaling; (iii) to determine whether heterologous type III effectors from pathogens of Arabidopsis suppress Pph-induced defense signaling, and (iv) to ascertain how basal defenses contribute to resistance against Pph by individually or multiply disrupting defense signaling pathways with mutations and heterologous type III effectors. We demonstrate that Pph elicits a minimum of three basal defense-signaling pathways in Arabidopsis. These pathways have unique readouts, including PR-1 protein accumulation and morphologically distinct types of callose deposition. Further, they require distinct defense genes, including PMR4, RAR1, SID2, NPR1, and PAD4. Finally, they are suppressed differentially by heterologous type III effectors, including AvrRpm1 and HopM1. Pph growth is enhanced only when multiple defense pathways are disrupted. For example, mutation of NPR1 or SID2 combined with the action of AvrRpm1 and HopM1 renders Arabidopsis highly susceptible to Pph. Thus, non-host resistance of Arabidopsis to Pph is based on multiple, individually effective layers of basal defense.

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