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Review
. 2020 Jan 22;21(3):716.
doi: 10.3390/ijms21030716.

Methyl Jasmonate Induced Oxidative Stress and Accumulation of Secondary Metabolites in Plant Cell and Organ Cultures

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Free PMC article
Review

Methyl Jasmonate Induced Oxidative Stress and Accumulation of Secondary Metabolites in Plant Cell and Organ Cultures

Thanh-Tam Ho et al. Int J Mol Sci. .
Free PMC article

Abstract

Recently, plant secondary metabolites are considered as important sources of pharmaceuticals, food additives, flavours, cosmetics, and other industrial products. The accumulation of secondary metabolites in plant cell and organ cultures often occurs when cultures are subjected to varied kinds of stresses including elicitors or signal molecules. Application of exogenous jasmonic acid (JA) and methyl jasmonate (MJ) is responsible for the induction of reactive oxygen species (ROS) and subsequent defence mechanisms in cultured cells and organs. It is also responsible for the induction of signal transduction, the expression of many defence genes followed by the accumulation of secondary metabolites. In this review, the application of exogenous MJ elicitation strategies on the induction of defence mechanism and secondary metabolite accumulation in cell and organ cultures is introduced and discussed. The information presented here is useful for efficient large-scale production of plant secondary metabolites by the plant cell and organ cultures.

Keywords: antioxidant enzyme activity; elicitor; methyl jasmonate; secondary metabolite; signal molecules.

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
The experimental process of Polygonum multiflorum for enhanced production of secondary metabolites.
Figure 2
Figure 2
Jasmonic acid and its derivatives.
Figure 3
Figure 3
General mechanism after MJ perception. Abbreviations: ROS reactive oxygen species, SA salicylic acid, JA jasmonic acid, ET ethylene, O2 superoxide anion, •OH hydroxyl radical, H2O2 hydrogen peroxide, SOD superoxide dismutase, CAT catalase, G-POD Guaiacol peroxidase, APX ascorbate peroxidase.
Figure 4
Figure 4
Effect of MJ on malondialdehyde (MDA) content (A), and antioxidant enzyme activity (B,C) in adventitious root cultures of Cnidium officinale. SOD superoxide dismutase, CAT catalase, G-POD guaiacol peroxidase, APX ascorbate peroxidase. Values represent mean ± SE (n = 3).
Figure 5
Figure 5
Schematic illustration of the sequential signalling pathways activated in elicited ginseng (A). Model of cross-talk between different signal transductions (B). Cross talk between different signalling molecules is shown by bold arrows. ACC 1-aminocyclopropane-1-carboxylic acid, ACS 1-aminocyclopropane-1-carboxylic acid synthase, ACO 1-aminocyclopropane-1-carboxylic acid, AOS allene oxide synthase, β-AS beta-amyrin synthase, DDS dammarenediol synthase, 12,13-EOT 12,13(S)-epoxyoctadecatrienoic acid, H2O2 hydrogen peroxide, 13-HPOT (13S)-hydroperoxyoctadecatrienoic acid, JA jasmonic acid, LOX lipoxygenase, NO nitric oxide, NOS nitric oxide synthase, O2 superoxide radical, OPR oxophytodienoate reductase, PLA phospholipase, SS squalene synthase, SE squalene epoxidase, TFs transcription factors, UGRdGT UDPG/ginsenoside Rd glucosyltransferase (Adapted from Rahimi et al. [5]).
Figure 6
Figure 6
Effect of MJ on phenolic compounds production in Cnidium officinale adventitious root culture.
Figure 7
Figure 7
Effect of MJ on biomass production in Polygonum multiflorum and Echinacea purpurea adventitious root culture system. (A,B) control and 100 µM MJ in P. multiflorum, (C,D) control and 100 µM MJ in E. purpurea, respectively.
Figure 8
Figure 8
Andrographolide biosynthetic gene activation by MJ elicitation in Andrographis paniculata [91]. Dashed blue arrows show the relationship between MJ signalling and andrographolide biosynthetic genes. HMG-CoA, 3-Hydroxy-3-methylglutaryl CoA. MVA, mevalonic acid. MVAP, mevalonic acid 5-phosphate. MVAPP, mevalonic acid 5-diphosphate. IPP, isopentenyl diphosphate. DMAPP, dimethylallyl diphosphate. MEP, 2-C-methyl-D-erythritol 4-phosphate. CDP-ME, 4-diphosphocytidyl-2-C-methyl-d-erythritol. CDP-MEP, 4-diphosphocytidyl2-C-methyl-D-erythritol 2-phosphate. ME-cPP, 2-C-methyl-D-erythritol 2,4-cyclodiphosphate. HMBPP, 1-hydroxy-2-methyl-2-(E)-butenyl 4-diphosphate. Enzymes of the MVA pathway: HMGS, HMG-CoA synthase. HMGR, HMG-CoA reductase. MVK, MVA kinase. PMK, MVAP kinase. PMD, MVAPP decarboxylase. Enzymes of the MEP pathway: DXS, DOXP synthase. DXR, DOXP reductoisomerase. CMS, CDP-ME synthase. CMK, CDP-ME kinase. MCS, ME-2,4cPP synthase. HDS, HMBPP synthase. HDR, HMBPP reductase, ISPH, 1-Hydroxy-2-methyl-2-(E)-butenyl 4-diphosphate reductase.

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