Disease relevance of Methyljasmonate

• We provide here a detailed analysis of the expression profiles of this group of Arabidopsis UGTs following infection with Pseudomonas syringae pv tomato or after treatment with salicylic acid, methyljasmonate, and hydrogen peroxide [1].
• Several myeloid leukemia cells were cultured with methyl jasmonate (MJ) and its derivatives [2].
• Finally, mice bearing EL-4 lymphoma and treated with MJ, survived for significantly (P = 0.00953) longer periods of time than untreated mice [3].

High impact information on Methyljasmonate

• Treatment of plants with methyl jasmonate (MeJA) increased the total binding of [(3)H]-l-volicitin to the enriched plasma membrane more than threefold, suggesting that MeJA activates transcription of the gene encoding the binding protein [4].
• In contrast to previous reports, no major increase in jasmonic acid (JA) and methyl jasmonate (MJ) was detected after the activation of SIPK/WIPK in NtMEK2DD transgenic plants [5].
• The antisense plants do produce both PG activity and H2O2 when supplied with systemin, OGA, chitosan, or MJ [6].
• In leaves of wild-type plants, NPR4 mRNA levels increase following pathogen challenge or SA treatment, and decrease rapidly following methyl jasmonic acid (MeJA) treatment [7].
• Expression of the jasmonic acid-dependent pathway marker gene PDF1.2 is compromised in npr4-1 leaves following application of MeJA or a combination of SA and MeJA [7].

Biological context of Methyljasmonate

• The mutation, termed ore4-1, delays a broad spectrum of age-dependent leaf senescence, but has little effect on leaf senescence artificially induced by darkness, abscisic acid (ABA), methyl jasmonate (MeJA), or ethylene [8].
• Orca3 mRNA accumulation was rapidly induced by the plant stress hormone methyljasmonate with biphasic kinetics [9].
• Furthermore, the 'conditioning' of developmental upregulation in flowers, the response to MeJa in flowers and leaves, and the parenchyma-specific expression are all mediated by the cis-elements within the proximal 192 bp of the promoter [10].
• A competitive inhibitor of ethylene (2,5-norbornadiene; NBD) down-regulated the effect of MeJA on sporamin gene expression [11].
• These data demonstrate that the promoter regions used in these experiments contain cis-acting regulatory elements required for proper regulation of tomlox expression during development and for MeJa-responsiveness [12].

Anatomical context of Methyljasmonate

• MJ also induced the differentiation of other human leukemia cell lines [2].
• MJ induced both monocytic and granulocytic differentiation of HL-60 cells [2].
• Aggregated suspension cultures, protoplasts, and single cells did not show any change in total protein content following elicitation with MJ at 200 microM on day 7 [13].
• A change in total enzyme activity in cultured cells was observed only at the highest concentration of MeJ and not at any level of ASA tested [14].
• It appears that while prolonged exposures to relatively low concentrations of jasmonates induce growth arrest and re-differentiation in myeloid leukemia cells, higher concentrations of MJ induce direct perturbation of cancer cell mitochondria, leading to the release of cytochrome c and eventual cell death [15].

Associations of Methyljasmonate with other chemical compounds

• Analysis of UGT expression in Arabidopsis defense-signaling mutants further revealed that their induction is methyljasmonate independent, but partially salicylic acid dependent [1].
• Glucosinolate content was analyzed in Arabidopsis wild-type plants in response to single or combinatorial treatments with methyljasmonate (MeJA), 2,6-dichloro-isonicotinic acid, ethylene, and 2,4-dichloro-phenoxyacetic acid, or by wounding [16].
• Moreover, eds4-1 and eds8-1 showed reduced expression of the plant defensin gene PDF1.2 after MeJA and ACC treatment, which was associated with reduced sensitivity to either ET (eds4-1) or MeJA (eds8-1) [17].
• In addition, an appreciable increase in phenylalanine ammonia-lyase activity occurred only in methyl-jasmonate-treated cell cultures of H. androsaemum [18].
• In contrast, when leaf senescence was induced by ethylene, ABA or methyljasmonate, the transcript level detected by the clones was differentially regulated depending on the senescence-inducing hormones [19].

Gene context of Methyljasmonate

• Transcripts of OPR3 rapidly accumulated in leaves after wounding and MeJA treatment, but they were detected in various tissues of unwounded plants at relatively low levels [20].
• MJ activated mitogen-activated protein kinase (MAPK) in the cells before causing myelomonocytic differentiation [2].
• MAPK activation was necessary for MJ-induced differentiation, since PD98059, an inhibitor of MAPK kinase, suppressed the differentiation induced by MJ [2].
• Shoot-applied MeJA strongly suppressed nodulation in the wild type and even hypernodulation in the har1 mutant, whereas MeSA exhibited no effect [21].
• Trans-2-hexenal induction thus closely mimics the group of genes induced by methyl jasmonate (MeJA), also a LOX-derived volatile [22].

Analytical, diagnostic and therapeutic context of Methyljasmonate

• The expression of both genes was up-regulated by addition of MJ to the cell cultures although the mRNA level of CaUGT1 was much lower than that of CaUGT2 [23].
• A general responsiveness in methyl-jasmonate-treated leaves was demonstrated by in situ hybridization [24].
• After screening various signal transducers, it was clear that methyl jasmonate (MeJA) markedly promoted saikosaponin production [25].
• The high-performance liquid chromatography (HPLC) profile of LCOs isolated following treatment with jasmonates or genistein showed that both JA and MeJA effectively induced nod genes and caused production of LCOs from bacterial cultures [26].

References