Be mediated by the higher levels of JAZ7 titrating out transcriptional repressors including JAM1. JAM1, JAM2 and JAM3 bind exactly the same DNA motif (G-box, CACGTG) as MYC2, MYC3 and MYC4 (Nakata et al., 2013; Fonseca et al., 2014), and through competitive binding for the identical DNA-binding web-site, these transcriptional repressors and activators can fine-tune JA-mediated responses. An unbiased in silico search (TAIR motif analysis: Statistical Motif Analysis in Promoter or Upstream Gene Sequences, 1000 bp) for G-box motifs (Dombrecht et al., 2007; Fernandez-Calvo et al., 2011) in the promoters in the up-regulated genes in jaz7-1D (Supplementary Table S5) identified 19 to include the CACGTG G-box motif, and2384 | Thatcher et al.and 38 to include the MYC2 binding variants CACATG and CACGTT, respectively (Dombrecht et al., 2007). The promoters of down-regulated jaz7-1D (Supplementary Table S6) genes also contained these motifs (CACGTG: 7; CACATG: 8; CACGTT: 4). These findings recommend JAZ7 co-ordinates the expression of stress-responsive genes via its interaction with certain MYC or JAM transcription variables and their binding to G-box DNA motifs. The ZIM domain of JAZ proteins mediates their homo- or heterodimerization (Chini et al., 2009; Chung and Howe, 2009; Chung et al., 2009), but JAZ7 appears to be the only JAZ protein incapable of homodimerizing or forming heterodimers with other JAZ proteins (Chini et al., 2009; Chung and Howe, 2009; reviewed by Pauwels and Goossens, 2011). An additional TIFYcontaining protein not capable of Eicosatetraynoic acid site interacting with JAZ proteins will be the non-JAZ protein TIFY8 (Cu lar P ez et al., 2014). Although TIFY8 has a functional ZIM domain that mediates transcriptional repression by recruiting TPL through NINJA, its ZIM domain will not confer interactions with JAZ proteins. The differences in JAZ7 protein-protein interactions recommend JAZ7 will not function just like the other JAZ repressors. Further to this, even though Jas and ZIM motifs in JAZ7 and JAZ8 are comparable, suggestive of similar binding activity (Shyu et al., 2012; Wager and Browse, 2012), they regulate binding to diverse transcription things. By way of example, we discovered JAZ7 and JAZ8 interacted with MYC34 and JAM1, but only JAZ8 interacted with MYC2. JAZ8 but not JAZ7, also interacts with JAM2 (Song et al., 2013; Fonseca et al., 2014), with two regulators of stamen development (MYB21 and MYB24) (Song et al., 2011) and with WD-repeatbHLHMYB complex members that regulate anthocyanin biosynthesis and trichome initiation (EGL3, GL3, TT8, MYB75, GL1, TTG1) (Qi et al., 2011). These variations in transcription factor binding may explain why JAZ8 overexpression confers decreased JA-sensitivity (Shyu et al., 2012) while high levels of JAZ7 in jaz7-1D plants confers enhanced JA-sensitivity (this operate). In summary, our outcomes assistance a model in which F. oxysporum stimulates JA-signaling, resulting in improved JAZ7 expression and JAZ7-TPL-mediated repression contributing to the manage of JA- responses and disease progression. Our characterization with the jaz7-1D mutant suggests the ectopic or non-wild-type high levels of JAZ7 in jaz7-1D can be a major determinant of its phenotypes and that these abnormal levels might be detrimental to the regular COI1-JAZ-TPL-MYCJAM regulatory network leading to hyperactivation of JA-signaling (Fig. 14B). Moreover, the unusual protein binding properties of JAZ7 in comparison to other JAZs may possibly exacerbate this phenotype (e.g. lack of homo- or heterodimerization, dive.
