Arabidopsis WRKY33 Is a Key Transcriptional Regulator of Hormonal and Metabolic Responses toward <i>Botrytis cinerea</i> Infection

  • Rainer P. Birkenbihl
    Department of Plant Microbe Interactions, Max Planck Institute for Plant Breeding Research, Cologne 50829, Germany (R.P.B., I.E.S.); Department of Molecular Ecology, Max Planck Institute for Chemical Ecology, Beutenberg Campus, Jena 07745, Germany (C.D.)
  • Celia Diezel
    Department of Plant Microbe Interactions, Max Planck Institute for Plant Breeding Research, Cologne 50829, Germany (R.P.B., I.E.S.); Department of Molecular Ecology, Max Planck Institute for Chemical Ecology, Beutenberg Campus, Jena 07745, Germany (C.D.)
  • Imre E. Somssich
    Department of Plant Microbe Interactions, Max Planck Institute for Plant Breeding Research, Cologne 50829, Germany (R.P.B., I.E.S.); Department of Molecular Ecology, Max Planck Institute for Chemical Ecology, Beutenberg Campus, Jena 07745, Germany (C.D.)

抄録

<jats:title>Abstract</jats:title> <jats:p>The Arabidopsis (Arabidopsis thaliana) transcription factor WRKY33 is essential for defense toward the necrotrophic fungus Botrytis cinerea. Here, we aimed at identifying early transcriptional responses mediated by WRKY33. Global expression profiling on susceptible wrky33 and resistant wild-type plants uncovered massive differential transcriptional reprogramming upon B. cinerea infection. Subsequent detailed kinetic analyses revealed that loss of WRKY33 function results in inappropriate activation of the salicylic acid (SA)-related host response and elevated SA levels post infection and in the down-regulation of jasmonic acid (JA)-associated responses at later stages. This down-regulation appears to involve direct activation of several jasmonate ZIM-domain genes, encoding repressors of the JA-response pathway, by loss of WRKY33 function and by additional SA-dependent WRKY factors. Moreover, genes involved in redox homeostasis, SA signaling, ethylene-JA-mediated cross-communication, and camalexin biosynthesis were identified as direct targets of WRKY33. Genetic studies indicate that although SA-mediated repression of the JA pathway may contribute to the susceptibility of wrky33 plants to B. cinerea, it is insufficient for WRKY33-mediated resistance. Thus, WRKY33 apparently directly targets other still unidentified components that are also critical for establishing full resistance toward this necrotroph.</jats:p>

収録刊行物

  • Plant Physiology

    Plant Physiology 159 (1), 266-285, 2012-03-05

    Oxford University Press (OUP)

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