Methyl jasmonate   中文名称: 茉莉酮酸甲酯

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.

[1]. The Anti-Proliferative and Anti-Invasive Effect of Leaf Extracts of Blueberry Plants Treated with Methyl Jasmonate on Human Gastric Cancer In Vitro Is Related to Their Antioxidant Properties. Antioxidants (Basel). 2020;9(1):45. Published 2020 Jan 4.

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

224.2961

224.141

1211-29-6

5281929

Colorless 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

43.37

0

3

6

16

281

2

CC/C=C\C[C@@H]1[C@H](CCC1=O)CC(=O)OC

GEWDNTWNSAZUDX-WQMVXFAESA-N

InChI=1S/C13H20O3/c1-3-4-5-6-11-10(7-8-12(11)14)9-13(15)16-2/h4-5,10-11H,3,6-9H2,1-2H3/b5-4-/t10-,11-/m1/s1

methyl 2-[(1R,2R)-3-oxo-2-[(Z)-pent-2-enyl]cyclopentyl]acetate

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)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

注意: 如下所列的是一些常用的体内动物实验溶解配方，主要用于溶解难溶或不溶于水的产品（水溶度<1 mg/mL）。 建议您先取少量样品进行尝试，如该配方可行，再根据实验需求增加样品量。

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注射用配方1: DMSO : Tween 80： Saline = 10 : 5 : 85 (如： 100 μL DMSO → 50 μL Tween 80 → 850 μL Saline)
*生理盐水/Saline的制备：将0.9g氯化钠/NaCl溶解在100 mL ddH ₂ O中，得到澄清溶液。
注射用配方 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL DMSO → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)
注射用配方 3: DMSO : Corn oil = 10 : 90 (如： 100 μL DMSO → 900 μL Corn oil)
示例: 以注射用配方 3 (DMSO : Corn oil = 10 : 90) 为例说明, 如果要配制 1 mL 2.5 mg/mL的工作液, 您可以取 100 μL 25 mg/mL 澄清的 DMSO 储备液，加到 900 μL Corn oil/玉米油中, 混合均匀。

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注射用配方 4: DMSO : 20% SBE-β-CD in Saline = 10 : 90 [如：100 μL DMSO → 900 μL (20% SBE-β-CD in Saline)]
*20% SBE-β-CD in Saline的制备（4°C，储存1周）：将2g SBE-β-CD (磺丁基-β-环糊精) 溶解于10mL生理盐水中，得到澄清溶液。
注射用配方 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (如： 500 μL 2-Hydroxypropyl-β-cyclodextrin (羟丙基环胡精)→ 500 μL Saline)
注射用配方 6: DMSO : PEG300 : Castor oil : Saline = 5 : 10 : 20 : 65 (如： 50 μL DMSO → 100 μL PEG300 → 200 μL Castor oil → 650 μL Saline)
注射用配方 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (如： 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
注射用配方 8: 溶解于Cremophor/Ethanol (50 : 50), 然后用生理盐水稀释。
注射用配方 9: EtOH : Corn oil = 10 : 90 (如： 100 μL EtOH → 900 μL Corn oil)
注射用配方 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL EtOH → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)

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口服配方 1: 悬浮于0.5% CMC Na (羧甲基纤维素钠)
口服配方 2: 悬浮于0.5% Carboxymethyl cellulose (羧甲基纤维素)
示例: 以口服配方 1 (悬浮于 0.5% CMC Na)为例说明, 如果要配制 100 mL 2.5 mg/mL 的工作液, 您可以先取0.5g CMC Na并将其溶解于100mL ddH2O中，得到0.5%CMC-Na澄清溶液；然后将250 mg待测化合物加到100 mL前述 0.5%CMC Na溶液中，得到悬浮液。

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口服配方 3: 溶解于 PEG400 (聚乙二醇400)
口服配方 4: 悬浮于0.2% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 5: 溶解于0.25% Tween 80 and 0.5% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 6: 做成粉末与食物混合

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注意: 以上为较为常见方法，仅供参考， InvivoChem并未独立验证这些配方的准确性。具体溶剂的选择首先应参照文献已报道溶解方法、配方或剂型，对于某些尚未有文献报道溶解方法的化合物，需通过前期实验来确定（建议先取少量样品进行尝试），包括产品的溶解情况、梯度设置、动物的耐受性等。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。