Phospholipase-dependent signalling during the AvrRpm1- and AvrRpt2-induced disease resistance responses in Arabidopsis thaliana

Authors

  • Mats X. Andersson,

    1. Department of Plant and Environmental Sciences, Göteborg University, Box 461, SE-405 30 Göteborg, Sweden,
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  • Olga Kourtchenko,

    1. Department of Plant and Environmental Sciences, Göteborg University, Box 461, SE-405 30 Göteborg, Sweden,
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  • Jeffery L. Dangl,

    1. Department of Biology, Department of Microbiology and Immunology and Curriculum in Genetics, Carolina Center for Genomic Sciences, Coker Hall CB #3280, University of North Carolina, Chapel Hill, NC 27599, USA, and
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  • David Mackey,

    1. Department of Horticulture and Crop Science, Department of Plant Cellular and Molecular Biology, Program in Plant Molecular Biology and Biotechnology, Program in Molecular Cellular and Developmental Biology, The Ohio State University, Room 306C Kottman Hall, Columbus, OH 43210, USA
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  • Mats Ellerström

    Corresponding author
    1. Department of Plant and Environmental Sciences, Göteborg University, Box 461, SE-405 30 Göteborg, Sweden,
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(fax +46 31 773 2626; e-mail mats.ellerstrom@botany.gu.se).

Summary

Bacterial pathogens deliver type III effector proteins into plant cells during infection. On susceptible host plants, type III effectors contribute to virulence, but on resistant hosts they betray the pathogen to the plant's immune system and are functionally termed avirulence (Avr) proteins. Recognition induces a complex suite of cellular and molecular events comprising the plant's inducible defence response. As recognition of type III effector proteins occurs inside host cells, defence responses can be elicited by in planta expression of bacterial type III effectors. We demonstrate that recognition of either of two type III effectors, AvrRpm1 or AvrRpt2 from Pseudomonas syringae, induced biphasic accumulation of phosphatidic acid (PA). The first wave of PA accumulation correlated with disappearance of monophosphatidylinosotol (PIP) and is thus tentatively attributed to activation of a PIP specific phospholipase C (PLC) in concert with diacylglycerol kinase (DAGK) activity. Subsequent activation of phospholipase D (PLD) produced large amounts of PA from structural phospholipids. This later wave of PA accumulation was several orders of magnitude higher than the PLC-dependent first wave. Inhibition of phospholipases blocked the response, and feeding PA directly to leaf tissue caused cell death and defence-gene activation. Inhibitor studies ordered these events relative to other known signalling events during the plant defence response. Influx of extracellular Ca2+ occurred downstream of PIP-degradation, but upstream of PLD activation. Production of reactive oxygen species occurred downstream of the phospholipases. The data presented indicate that PA is a positive regulator of RPM1- or RPS2-mediated disease resistance signalling, and that the biphasic PA production may be a conserved feature of signalling induced by the coiled-coil nucleotide binding domain leucine-rich repeat class of resistance proteins.

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