Role of NINJA in root jasmonate signaling

Abstract

Wound responses in plants have to be coordinated between organs so that locally reduced growth in a wounded tissue is balanced by appropriate growth elsewhere in the body. We used a JASMONATE ZIM DOMAIN 10 (JAZ10) reporter to screen for mutants affected in the organ-specific activation of jasmonate (JA) signaling in Arabidopsis thaliana seedlings. Wounding one cotyledon activated the reporter in both aerial and root tissues, and this was either disrupted or restricted to certain organs in mutant alleles of core components of the JA pathway including COI1, OPR3, and JAR1. In contrast, three other mutants showed constitutive activation of the reporter in the roots and hypocotyls of unwounded seedlings. All three lines harbored mutations in Novel Interactor of JAZ (NINJA), which encodes part of a repressor complex that negatively regulates JA signaling. These ninja mutants displayed shorter roots mimicking JA-mediated growth inhibition, and this was due to reduced cell elongation. Remarkably, this phenotype and the constitutive JAZ10 expression were still observed in backgrounds lacking the ability to synthesize JA or the key transcriptional activator MYC2. Therefore, JA-like responses can be recapitulated in specific tissues without changing a plant's ability to make or perceive JA, and MYC2 either has no role or is not the only derepressed transcription factor in ninja mutants. Our results show that the role of NINJA in the root is to repress JA signaling and allow normal cell elongation. Furthermore, the regulation of the JA pathway differs between roots and aerial tissues at all levels, from JA biosynthesis to transcriptional activation. root growth | herbivory | plant fertility | mapping by sequencing

Phosphate Deficiency Induces the Jasmonate Pathway and Enhances Resistance to Insect Herbivory

“…1C). The expression of JAZ10 in both shoots and roots of plants grown in high or low Pi was strongly reduced in the JA biosynthetic mutant aos lacking allene oxidase activity (Park et al, 2002) and the JA signaling mutant coi1-34 (a fertile allele of coi1; Acosta et al, 2013;Fig. 1, A and B).…”

“…The aos, coi1-1, coi1-34, and pho1-2 mutants were described previously (Feys et al, 1994;Hamburger et al, 2002;Park et al, 2002;Acosta et al, 2013). The gl1 mutation present in the original coi1-1 mutant (Feys et al, 1994) was removed by backcrossing and was used in all experiments (provided by Jane Glazebrook, University of Minnesota).…”

Interaction between MYC2 and ETHYLENE INSENSITIVE3 Modulates Antagonism between Jasmonate and Ethylene Signaling inArabidopsis

“…Upon perception of JA signal (Fonseca et al, 2009;Yan et al, 2009;Sheard et al, 2010), the F-box protein CORO-NATINE INSENSITIVE1 (COI1) (Xie et al, 1998;Yan et al, 2009) recruits the JASMONATE ZIM-DOMAIN (JAZ) proteins (Chini et al, 2007;Thines et al, 2007;Yan et al, 2007) for degradation, which leads to the release of various downstream factors, including MYC2/JASMONATE INSENSITIVE1 (JIN1), MYC3, and MYC4 (Cheng et al, 2011;Fernández-Calvo et al, 2011;Niu et al, 2011), as well as WD-repeat/bHLH/MYB complex , MYB21, MYB24, and MYB57 (Mandaokar et al, 2006;Song et al, 2011) and the IIId bHLH factors (Nakata et al, 2013;Song et al, 2013b), which regulate diverse JA-mediated functions. These functions include root growth (Dathe et al, 1981;Chen et al, 2011), apical hook formation (Turner et al, 2002), flowering (Robson et al, 2010), stamen development (McConn and Browse, 1996;Song et al, 2011Song et al, , 2013a, leaf senescence (Ueda and Kato, 1980;Shan et al, 2011), secondary metabolism (De Geyter et al, 2012;Schweizer et al, 2013), drought responses (Seo et al, 2011), wounding responses (Mason and Mullet, 1990;Acosta et al, 2013;Mousavi et al, 2013), and defense against pathogen infection Vijayan et al, 1998;Melotto et al, 2006;Rowe et al, 2010;Yang et al, 2012;Zheng et al, 2012) and insect attack (McConn et al, 1997;…”

Structural insights into alternative splicing-mediated desensitization of jasmonate signaling

“…Second, JAZ proteins recruit members of the TOPLESS (TPL) class of corepressors either through direct binding of TPL to ethylene-response factor-associated amphiphilic repression (EAR) motifs found at the N terminus of a subset of JAZ proteins or indirectly through the EAR motif-containing NINJA adaptor protein that binds to the central ZIM domain of JAZ proteins (Fig. 1A) (12)(13)(14)(15)(16). TPL proteins in turn recruit repressive histone deacetylases and chromatin remodelers (17,18) to inhibit MYC target gene expression epigenetically.…”