Oposed mode of JA-hyper-activation in jaz7-1D plants. (A) JAZ7 domain structure highlighting the N-terminal EAR motif, ZIM and Jas domains, in addition to a comparison against conserved JAZ interaction domains in JAZ1. The EAR motif, TIFY motif and JAZ degron for the ZIM and Jas domains respectively are underlined. Residues in the JAZ1 Jas motif shown in bold red are expected for Chroman 1 Autophagy COI1-binding. In JAZ1, the ZIM domain mediates NINJA binding and JAZ homo- and heterodimerization, plus the Jas domain mediates COI1 binding and interactions with various transcription factors. (B) Proposed model for JA-responses in jaz7-1D plants. Through its EAR domain, JAZ7 binds using the co-repressor TPL to facilitate transcriptional repression. High levels of JAZ7 are related with hyper-activation of JA-signaling possibly via JAZ7 disturbing components of this network (e.g. TPL, JAM1).T-DNA insertion lines in JAZ genes for altered F. oxysporum illness phenotypes. Though most overexpression or knockout lines of person JAZ genes lack observable JA-related phenotypes, suggesting functional redundancy amongst the JAZ proteins (reviewed in Wasternack and Hause, 2013), we identified the jaz7-1D T-DNA insertional activation mutant which conferred hyper-activation of JA-signaling such as up-regulation of JA-regulated biosynthesis, defense and senescence-associated genes (Fig. 8), too as up-regulation of most other JAZ genes (Fig. 9). In an unbiased approach to recognize genes differentially regulated in jaz7-1D, our microarray analysis identified genes up-regulated 2-fold in jaz7-1D more than wild-type to be considerably enriched for involvement in pressure and defense responses. By far the most very up-regulated gene (9.5-fold) NATA1 in the jaz7-1D mutant encodes a N-acetyltransferase, which acetylates ornithine to produce the defense-related metabolite N-acetylornithine. Yan et al. (2014) also found this metabolite is more abundant in SALK_040835 (jaz7-1D) and its levels are highly up-regulated more than wild-type following MeJA remedy. NATA1 expression is hugely responsive to JA, Pst and herbivory (Adio et al., 2011) plus a knockout mutant of NATA1 has increased resistance to Pst DC3000 (Adio et al., 2011), supporting our benefits for jaz7-1D. Adio et al. (2011) suggest that Pst DC3000 infection is promoted by coronatineMeJAinduced expression of NATA1 and subsequent production of N-acetylornithine. Although Thi2.1, the second most highly up-regulated gene in jaz7-1D, has been linked to increased F. oxysporum resistance (Epple et al., 1997; Chan et al., 2005; Thatcher et al., 2012a), Thi2.1 just isn’t a single determinant ofF. oxysporum resistance. Indeed, other mutants with constitutive Thi2.1 expression (e.g. cpr5) are very susceptible although coi1 plants with severely compromised Thi2.1 expression are extremely resistant (Bowling et al., 1997; Schenk et al., 2005; Thatcher et al., 2009). Another gene extremely up-regulated in jaz7-1D was Histone1-3 (HIS1-3). HIS1-3 encodes a linker histone which functions as a stabilizer of chromatin structure and its expression is extremely drought inducible, suggestive of a role in tension tolerance (Ascenzi and Gantt, 1999). Lately it was found that JAZ7 plays a role in Pyrroloquinoline quinone Endogenous Metabolite adverse regulation of dark-induced leaf senescence (Yu et al., 2015). By means of analysis on the jaz7-1 (WiscDsLox7H11) knockout line, Yu and colleagues located senescence and H2O2-mediated responses and genes involved in these processes like NATA1 and DIN11 have been significantly.
