The<i>Arabidopsis</i>bHLH Transcription Factors MYC3 and MYC4 Are Targets of JAZ Repressors and Act Additively with MYC2 in the Activation of Jasmonate Responses  

Patricia Fernández‐Calvo(Consejo Superior de Investigaciones Científicas), Andrea Chini(Consejo Superior de Investigaciones Científicas), Gemma Fernández‐Barbero(Consejo Superior de Investigaciones Científicas), José-Manuel Chico(Consejo Superior de Investigaciones Científicas), Selena Giménez-Ibañez(Consejo Superior de Investigaciones Científicas), Jan Geerinck(Ghent University), Dominique Eeckhout(Ghent University), Fabian Schweizer(University of Lausanne), Marta Godoy(Consejo Superior de Investigaciones Científicas), José M. Franco‐Zorrilla(Consejo Superior de Investigaciones Científicas), Laurens Pauwels(Ghent University), Erwin Witters(University of Antwerp), María Isabel Puga(Consejo Superior de Investigaciones Científicas), Javier Paz‐Ares(Consejo Superior de Investigaciones Científicas), Alain Goossens(Ghent University), Philippe Reymond(University of Lausanne), Geert De Jaeger(Ghent University), Roberto Solano(Consejo Superior de Investigaciones Científicas)
The Plant Cell
February 1, 2011
Cited by 1,170Open Access
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Abstract

Jasmonates (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.


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