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The transcription factor MYC2 has emerged as a master regulator of jasmonate (JA)-mediated responses as well as crosstalk among different signaling pathways. The instability of MYC2 is in part due to the action of PUB10 E3 ligase, which can polyubiquitinate this protein. Here, we show that polyubiquitinated MYC2 can be deubiquitinated by UBP12 and UBP13 in vitro, suggesting that the two deubiquitinating enzymes can counteract the effect of PUB10 in vivo. Consistent with this view, UBP12 and UBP13 associate with MYC2 in the nucleus. Transgenic Arabidopsis thaliana plants deficient in UBP12 and UBP13 show accelerated decay of MYC2 and are hyposensitive to JA , whereas plants overexpressing UBP12 or UBP13 have prolonged MYC2 half-life and are hypersensitive to JA. Our results suggest that there is a genetic link between UBP12, UBP13, and MYC2. Our results identify UBP12 and UBP13 as additional positive regulators of JA responses and suggest that these enzymes likely act by stabilizing MYC2. [ABSTRACT FROM AUTHOR]

Volatile organic compounds (VOCs) easily diffuse due to their high hydrophobicity. Because of this physical property, VOCs are able to act as crucial signalling molecules mediating intercellular and interplant communication. Methyl jasmonate (MeJA) is a volatile ester form of jasmonic acid (JA) that is involved in interplant communication in response to biotic and abiotic stresses. Despite its function in interplant communication, the specific role of MeJA in the regulation of intercellular jasmonate responses have been poorly understood. In this study, we demonstrated that MeJA is much more effective than JA in inducing jasmonate response, and the higher efficacy of MeJA relies on its volatile property. To understand the function of MeJA in the regulation of the jasmonate response, we analysed function of JMT gene, Jasmonic acid Methyl Transferase using its knockout mutant ( jmt) and overexpressing plants ( 35S:JMT). Mutant plants that lack JMT expression exhibited reduced jasmonate response, while JMT-overexpressing plants exhibited a higher jasmonate response to JA treatment compared to wild-type plants. In this study, we also showed that JMT is specifically expressed in the phloem, the main vascular system for the transport of phytohormones, and that JMT expression affects systemic jasmonate response in wounding. These results suggest the volatile MeJA is a transmissible form of jasmonate and that its biosynthesis is involved in systemic jasmonate response in wounding. [ABSTRACT FROM AUTHOR]

Jasmonates (JAs) are important regulators of plant biotic and abiotic stress responses and development. AtJMT in Arabidopsis thaliana and BcNTR1 in Brassica campestris encode jasmonic acid carboxyl methyltransferases, which catalyze methyl jasmonate (MeJA) biosynthesis and are involved in JA signaling. Their expression is induced by MeJA application. To understand its regulatory mechanism, here we define a novel JA-responsive cis-element (JARE), G(C)TCCTGA, in the AtJMT and BcNTR1 promoters, by promoter deletion analysis and Yeast 1-Hybrid (Y1H) assays; the JARE is distinct from other JA-responsive cis-elements previously reported. We also used Y1H screening to identify a trans-acting factor, AtBBD1, which binds to the JARE and interacts with AtJAZ1 and AtJAZ4. Knockout and overexpression analyses showed that AtBBD1 and its close homologue AtBBD2 are functionally redundant and act as negative regulators of AtJMT expression. However, AtBBD1 positively regulated the JA-responsive expression of JR2. Chromatin immunoprecipitation from knockout and overexpression plants revealed that repression of AtJMT is associated with reduced histone acetylation in the promoter region containing the JARE. These results show that AtBBD1 interacts with JAZ proteins, binds to the JARE and represses AtJMT expression. [ABSTRACT FROM AUTHOR]