TheArabidopsisbHLH Transcription Factors MYC3 and MYC4 Are Targets of JAZ Repressors and Act Additively with MYC2 in the Activation of Jasmonate Responses

Author:

Fernández-Calvo Patricia1,Chini Andrea1,Fernández-Barbero Gemma1,Chico José-Manuel1,Gimenez-Ibanez Selena1,Geerinck Jan23,Eeckhout Dominique23,Schweizer Fabian4,Godoy Marta5,Franco-Zorrilla José Manuel5,Pauwels Laurens23,Witters Erwin67,Puga María Isabel1,Paz-Ares Javier1,Goossens Alain23,Reymond Philippe4,De Jaeger Geert23,Solano Roberto15

Affiliation:

1. Departamento de Genética Molecular de Plantas, Centro Nacional de Biotecnología–Consejo Superior de Investigaciones Científicas, Campus Universidad Autónoma, 28049 Madrid, Spain

2. Department of Plant Systems Biology, VIB, B-9052 Ghent, Belgium

3. Department of Plant Biotechnology and Genetics, Ghent University, B-9052 Ghent, Belgium

4. Department of Plant Molecular Biology, University of Lausanne, CH-1015 Lausanne, Switzerland

5. Genomics Unit, Centro Nacional de Biotecnología–Consejo Superior de Investigaciones Científicas, Campus Universidad Autónoma, 28049 Madrid, Spain

6. Department of Biology, EBT-CEPROMA, University of Antwerp, B-2020 Antwerpen, Belgium

7. Flemish Institute for Technological Research, VITO-MANT, B-2400 Mol, Belgium

Abstract

AbstractJasmonates (JAs) trigger an important transcriptional reprogramming of plant cells to modulate both basal development and stress responses. In spite of the importance of transcriptional regulation, only one transcription factor (TF), the Arabidopsis thaliana basic helix-loop-helix MYC2, has been described so far as a direct target of JAZ repressors. By means of yeast two-hybrid screening and tandem affinity purification strategies, we identified two previously unknown targets of JAZ repressors, the TFs MYC3 and MYC4, phylogenetically closely related to MYC2. We show that MYC3 and MYC4 interact in vitro and in vivo with JAZ repressors and also form homo- and heterodimers with MYC2 and among themselves. They both are nuclear proteins that bind DNA with sequence specificity similar to that of MYC2. Loss-of-function mutations in any of these two TFs impair full responsiveness to JA and enhance the JA insensitivity of myc2 mutants. Moreover, the triple mutant myc2 myc3 myc4 is as impaired as coi1-1 in the activation of several, but not all, JA-mediated responses such as the defense against bacterial pathogens and insect herbivory. Our results show that MYC3 and MYC4 are activators of JA-regulated programs that act additively with MYC2 to regulate specifically different subsets of the JA-dependent transcriptional response.

Publisher

Oxford University Press (OUP)

Subject

Cell Biology,Plant Science

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