Up-regulated in Methyl palmitoleate Protocol jaz7-1 in darkness but not below light conditions. We identified no alteration in Fusarium-induced senescence responses or oxidative tension responsive gene expression in jaz7-1 in comparison to wild-type plants (Figs four, eight). Thus it seems JAZ7 plays contrasting roles in pathogen and dark-induced senescence responses. In addition to hyperactivation of JA-responses, the jaz71D mutant displayed an early flowering phenotype (Fig. six). Hyperlinks involving flowering time and altered JA-mediated pathogen resistance happen to be reported previously. As an example, the pft1med25 mutant is delayed in flowering, exhibits down-regulated JA-defense responses and increased resistance to F. oxysporum (Kidd et al., 2009). It has been shown COI1-dependent signaling delays flowering time by way of JAZ degradation and inhibiting the expression of FLOWERING LOCUS T (FT) (Zhai et al., 2015). Though increasedActivation-tagged jaz7-1D mutant confers susceptibility to Fusarium oxysporum |JA-signaling and JAZ expression is evident in jaz7-1D plants, we didn’t detect altered expression of FT in our microarray evaluation. However, other genes known to regulate flowering were altered (e.g. DET2DWF6). The constitutive activation of JA-signaling in jaz7-1D might also be responsible for its compact rosette phenotype and lowered root-length (Figs 2A, 7C). Many other mutants with constitutive JA-defense gene expression (e.g. cpr5, cev1, cet1, dnd1, dnd2) also show stunted development (Bowling et al., 1997; Ellis and Turner, 2001; Hilpert et al., 2001; Genger et al., 2008). Without the need of stringent regulation, continual activation of JA responses would place big demands on plant resources, repressing growth, and probably contribute to these dwarf phenotypes (Baldwin, 1998; Kazan and Manners, 2012; Pieterse et al., 2014). That is supported by the acquiring that defense and stress-related metabolites are improved in jaz7-1DSALK_040835C which might limit resources offered for growth (Yan et al., 2014). Basal expression of JA-marker genes in the JAZ7 overexpression lines (JAZ7-OX) that we generated was also improved, but not to the significantly high levels observed in jaz7-1D, and may perhaps account for why the JAZ7-OX lines didn’t exhibit the stunted jaz7-1D root and leaf phenotypes. To rule out the possibilities that altered JAZ7 transcripts (e.g. mutated, misspliced) or other T-DNA insertions in jaz7-1D are responsible for its JA-hyperactivation phenotypes, we performed various extra analyses and backcrossed jaz7-1D to wild-type plants. Our final results suggest the T-DNA insertion inside the JAZ7 promoter is associated with all the jaz7-1D phenotypes. However we can’t exclude the possibility that undetected secondary mutations or feasible chromosomal rearrangements resulting from T-DNA transformation may possibly contribute. For other JAZ proteins characterized to date, JA-related phenotypes like JA-insensitivity, sterility or altered tolerance to pathogens or pests have only been identified for JAZ8 and JAZ13 overexpressing lines (Shyu et al., 2012; Thireault et al., 2015), jaz10 T-DNA or RNAi knockdown lines (Cerrudo et al., 2012; Leone et al., 2014), or in modified JAZ proteins in which the conserved C-terminal Jas motif has been deleted or its essential amino acids modified. These alterations stabilize the JAZ protein by preventing its interaction with COI1 and subsequent ubiquitin-mediated degradation following JA-stimulation (Chini et al., 2007; Thines et al., 2007; Yan et al., 2007; Chung et al., 2008.
