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First published online January 25, 2008; 10.1104/pp.107.115691 Plant Physiology 146:952-964 (2008) © 2008 American Society of Plant Biologists OPEN ACCESS ARTICLE
Regulation and Function of Arabidopsis JASMONATE ZIM-Domain Genes in Response to Wounding and Herbivory1,[W],[OA]Department of Energy Plant Research Laboratory (H.S.C., A.J.K.K., S.J., G.A.H.), and Department of Biochemistry and Molecular Biology (H.S.C., X.G., A.D.J., G.A.H.), Michigan State University, East Lansing, Michigan 48824; and Institute of Biological Chemistry, Washington State University, Pullman, Washington 99164–6340 (B.T.)
Jasmonate (JA) and its amino acid conjugate, jasmonoyl-isoleucine (JA-Ile), play important roles in regulating plant defense responses to insect herbivores. Recent studies indicate that JA-Ile promotes the degradation of JASMONATE ZIM-domain (JAZ) transcriptional repressors through the activity of the E3 ubiquitin-ligase SCFCOI1. Here, we investigated the regulation and function of JAZ genes during the interaction of Arabidopsis (Arabidopsis thaliana) with the generalist herbivore Spodoptera exigua. Most members of the JAZ gene family were highly expressed in response to S. exigua feeding and mechanical wounding. JAZ transcript levels increased within 5 min of mechanical tissue damage, coincident with a large (approximately 25-fold) rise in JA and JA-Ile levels. Wound-induced expression of JAZ and other CORONATINE-INSENSITIVE1 (COI1)-dependent genes was not impaired in the jar1-1 mutant that is partially deficient in the conversion of JA to JA-Ile. Experiments performed with the protein synthesis inhibitor cycloheximide provided evidence that JAZs, MYC2, and genes encoding several JA biosynthetic enzymes are primary response genes whose expression is derepressed upon COI1-dependent turnover of a labile repressor protein(s). We also show that overexpression of a modified form of JAZ1 (JAZ1
1 This work was supported by the National Institutes of Health (grant GM57795), the U.S. Department of Energy (grant DE–FG02–91ER20021 to G.A.H.), and the U.S. Department of Energy (grant DE–FG02–99ER20323 to John Browse for B.T.). 2 Present address: San Luis Valley Research Center, 0249 East Rd. 9 North, Colorado State University, Center, CO 81125. The author responsible for distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instructions for Authors (www.plantphysiol.org) is: Gregg A. Howe (howeg{at}msu.edu). [W] The online version of this article contains Web-only data. [OA] Open Access articles can be viewed online without a subscription. www.plantphysiol.org/cgi/doi/10.1104/pp.107.115691 * Corresponding author; e-mail howeg{at}msu.edu. Received December 31, 2007; accepted January 21, 2008; published January 25, 2008. This article has been cited by other articles:
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3A) that is stable in the presence of JA compromises host resistance to feeding by S. exigua larvae. These findings establish a role for JAZ proteins in the regulation of plant anti-insect defense, and support the hypothesis that JA-Ile and perhaps other JA derivatives activate COI1-dependent wound responses in Arabidopsis. Our results also indicate that the timing of JA-induced transcription in response to wounding is more rapid than previously realized. 
