<i>JASMONATE-INSENSITIVE1</i>Encodes a MYC Transcription Factor Essential to Discriminate between Different Jasmonate-Regulated Defense Responses in Arabidopsis[W]

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  • Oscar Lorenzo
    Departamento de Geneética Molecular de Plantas, Centro Nacional de Biotecnologiéa, Consejo Superior de Investigaciones Cientificas, Campus Universidad Autoénoma, 28049 Madrid, Spain
  • Jose M. Chico
    Departamento de Geneética Molecular de Plantas, Centro Nacional de Biotecnologiéa, Consejo Superior de Investigaciones Cientificas, Campus Universidad Autoénoma, 28049 Madrid, Spain
  • Jose J. Saénchez-Serrano
    Departamento de Geneética Molecular de Plantas, Centro Nacional de Biotecnologiéa, Consejo Superior de Investigaciones Cientificas, Campus Universidad Autoénoma, 28049 Madrid, Spain
  • Roberto Solano
    Departamento de Geneética Molecular de Plantas, Centro Nacional de Biotecnologiéa, Consejo Superior de Investigaciones Cientificas, Campus Universidad Autoénoma, 28049 Madrid, Spain

Abstract

<jats:title>Abstract</jats:title><jats:p>In spite of the importance of jasmonates (JAs) as plant growth and stress regulators, the molecular components of their signaling pathway remain largely unknown. By means of a genetic screen that exploits the cross talk between ethylene (ET) and JAs, we describe the identification of several new loci involved in JA signaling and the characterization and positional cloning of one of them, JASMONATE-INSENSITIVE1 (JAI1/JIN1). JIN1 encodes AtMYC2, a nuclear-localized basic helix-loop-helix-leucine zipper transcription factor, whose expression is rapidly upregulated by JA, in a CORONATINE INSENSITIVE1–dependent manner. Gain-of-function experiments confirmed the relevance of AtMYC2 in the activation of JA signaling. AtMYC2 differentially regulates the expression of two groups of JA-induced genes. The first group includes genes involved in defense responses against pathogens and is repressed by AtMYC2. Consistently, jin1 mutants show increased resistance to necrotrophic pathogens. The second group, integrated by genes involved in JA-mediated systemic responses to wounding, is activated by AtMYC2. Conversely, Ethylene-Response-Factor1 (ERF1) positively regulates the expression of the first group of genes and represses the second. These results highlight the existence of two branches in the JA signaling pathway, antagonistically regulated by AtMYC2 and ERF1, that are coincident with the alternative responses activated by JA and ET to two different sets of stresses, namely pathogen attack and wounding.</jats:p>

Journal

  • The Plant Cell

    The Plant Cell 16 (7), 1938-1950, 2004-07-01

    Oxford University Press (OUP)

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