Interactions
Researchers investigated the effects of the combined action of methyl jasmonate and sucrose on the expression of defense-related genes, stilbene, and anthocyanin production in grape cell suspensions. Methyl jasmonate/sucrose treatment effectively stimulated the expression of genes for phenylalanine ammonia-lyase, chalcone synthase, stilbene synthase, UDP-glucose:flavonoid-O-glucosyltransferase, protease inhibitors, and chitinase, and induced the accumulation of spruce compounds and anthocyanins intracellularly, as well as the accumulation of trans-resveratrol and spruce compounds in extracellular culture medium…
Capsicum annuum suspension cell cultures were used to evaluate the effects of cyclodextrin and methyl jasmonate as inducers of defense responses. The induced defense responses included the accumulation of sesquiterpenes and phytosterols, as well as the activation of pathogenesis-related proteins, thereby enhancing and altering cell wall structure during induction and protecting cells from biotic stress. The results showed that the addition of both cyclodextrin and methyl jasmonate induced the biosynthesis of two sesquiterpenes—aromatic resins and soravidone. This response exhibits a significant synergistic effect, as the increase in the levels of these compounds is far greater when both inducers are present than when used alone. Phytosterol biosynthesis is also induced in the combined treatment due to an additive effect. Similarly, exogenous application of methyl jasmonate induces the accumulation of disease-related proteins. Extracellular proteomic analysis revealed the presence of amino acid sequences homologous to PR1 and PR4, NtPRp27-like proteins, class I chitinases, peroxidases, hydrolases LEXYL1 and LEXYL2, arabinosidases, pectinases, nectarin IV, and leucine-rich repeat proteins, indicating that methyl jasmonate mediates the expression of defense-related gene products in pepper (C. annuum). In addition to these methyl jasmonate-induced proteins, other PR proteins were found in both control and induced cell cultures of pepper. These enzymes, including class IV chitinases, β-1,3-glucanases, sweet protein-like enzymes, and peroxidases, indicate that their expression is primarily constitutive, as they are involved in plant growth, development, and defense processes. Boron is an essential micronutrient for plants, but excessive boron in the soil is phytotoxic to some plants, such as Artemisia annua, whose aerial parts contain artemisinin (an important antimalarial drug). Artemisinin is a sesquiterpene lactone with an internal peroxide bridge… This study aimed to determine whether exogenous application of methyl jasmonate (MeJA) could counteract the adverse effects of excessive boron stress (B) in the soil. Results showed that boron toxicity induced oxidative stress and significantly reduced stem height, fresh weight, and dry weight. Excess boron in the soil reduced net photosynthetic rate, stomatal conductance, intercellular carbon dioxide concentration, and total chlorophyll content in leaves. Conversely, foliar application of methyl jasmonate (MeJA) improved growth and photosynthetic efficiency in both stressed and unstressed plants. Excessive boron can also increase the activity of antioxidant enzymes (such as catalase, peroxidase, and superoxide dismutase)... Applying MeJA to stressed plants can reduce lipid peroxidation, stimulate the synthesis of antioxidant enzymes, and increase the content and yield of artemisinin. Therefore, it can be concluded that MeJA can be used to alleviate boron toxicity and increase the content and yield of artemisinin in Artemisia annua.

Methyl jasmonic acid (-) is a methyl ester derivative of jasmonic acid. It belongs to the jasmonic acid ester class and is a plant metabolite and plant hormone. It is a jasmonic acid ester, a methyl ester, and a member of the jasmonic acid ester derivative family. Methyl jasmonic acid has been reported to be present in potatoes (Solanum tuberosum), Tripterygium wilfordii, and other organisms with relevant data. Mechanism of Action: Using the pathogenic form of Alternaria alternata (Aa) and its AAL toxin/tomato interaction system as a model system, the authors demonstrated the potential role of jasmonic acid (JA) in plant susceptibility to pathogens that utilize host-specific toxins as virulence effectors. Compared to wild-type (WT) varieties, the def1 mutant with JA biosynthesis deficiency showed inhibited disease development and plant growth in Aa-pathogenic tomato plants. Exogenous application of methyl jasmonic acid (MeJA) restored pathogen symptoms in the def1 mutant and exacerbated the disease in WT plants. On the other hand, AAL toxin induced similar necrotic cell death in both def1 and WT plants, and MeJA application did not affect the degree of toxin-induced cell death. These results indicate that the JA-dependent signaling pathway does not participate in the host's basal defense response to Aa pathogens in tomato, but may affect pathogen tolerance in a toxin-independent manner. Further data suggest that jasmonic acid (JA) promotes the infection of both toxin-producing and necrotic pathogens in tomato, and that pathogens may utilize the JA signaling pathway for successful infection. ...WRKY is a plant-specific transcription factor and one of the flagellin-inducing genes in its non-host, Arabidopsis thaliana. Inoculation with the incompatible pathogen Pseudomonas syringae DC3000 (Pto) containing AvrRpt2 and non-host pathogens induced WRKY41 expression… Arabidopsis thaliana overexpressing WRKY41 showed enhanced resistance to wild-type Pto but increased susceptibility to Erwinia carotenoides EC1. Arabidopsis thaliana overexpressing WRKY41 constitutively expressed the PR5 gene but suppressed methyl jasmonic acid-induced PDF1.2 gene expression. These results suggest that WRKY41 may be a key regulator of the interaction between the salicylic acid and jasmonic acid signaling pathways.
Induced cell death is an important component of plant defense against pathogens. Numerous reports have documented the roles of plant hormones in pathogen-induced cell death, but jasmonic acid (JA) has not yet been identified as a regulator of this response. In this paper, researchers report the function of Nicotiana benthamiana homeobox 1 (NbHB1) in pathogen-induced cell death within the JA signaling pathway. The role of NbHB1 in cell death was analyzed through gain-of-function and loss-of-function experiments using Agrobacterium-mediated transient overexpression and virus-induced gene silencing, respectively. Reverse transcription polymerase chain reaction (RT-PCR) was used to monitor NbHB1 expression after pathogen inoculation and various treatments. Results showed that infection with both virulent and attenuated bacterial pathogens upregulated NbHB1 transcription levels. Ectopic expression of NbHB1 accelerated cell death after darkness, methyl jasmonate, or pathogen inoculation. Conversely, when NbHB1 was silenced, pathogen-induced cell death was delayed. Silencing of NbCOI1 also delayed NbHB1-induced cell death, indicating that the JA-mediated signaling pathway is essential. Overexpression of NbHB1 domain-deficient proteins indicated that the homologous domain, leucine zipper domain, and partially variable N-terminal region are essential for NbHB1 function. These results strongly suggest that NbHB1 plays a role in pathogen-induced plant cell death through the JA-mediated signaling pathway. In this study, the authors used high-throughput Illumina sequencing to identify miRNAs in Taxus chinensis cells to investigate the effect of the taxane inducer methyl jasmonic acid (MJ) on miRNA expression. In a dataset containing approximately 6.6 million sequences, 58 miRNAs belonging to 25 families were identified. Most of these were conserved in both angiosperms and gymnosperms. However, two miRNAs (miR1310 and miR1314) appeared to be gymnosperm-specific, with miR1314 possibly existing in clusters. MJ treatment significantly affected the expression of specific miRNAs; 14 miRNAs from 7 different families (miR156, miR168, miR169, miR172, miR396, miR480, and miR1310) were downregulated, while 3 miRNAs from 2 families (miR164 and miR390) were upregulated. For more complete data on the mechanisms of action of methyl jasmonate (13 in total), please visit the HSDB record page.

C13H20O3

224.30

224.141

39924-52-2

5281929

Colorless to light yellow liquid

1.0±0.1 g/cm3

302.9±15.0 °C at 760 mmHg

25 °C

128.6±20.4 °C

0.0±0.6 mmHg at 25°C

1.469

2.12

0

3

6

16

281

2

O=C1C([H])([H])C([H])([H])C([H])(C([H])([H])C(=O)OC([H])([H])[H])C1([H])C([H])([H])/C(/[H])=C(/[H])\C([H])([H])C([H])([H])[H]

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO: 100 mg/mL (445.83 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (11.15 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

---

Solubility in Formulation 2: ≥ 2.5 mg/mL (11.15 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

---

View More

Solubility in Formulation 3: ≥ 2.5 mg/mL (11.15 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

---

 (Please use freshly prepared in vivo formulations for optimal results.)