Plants metabolism affect nutritional availability depriving pathogens of its nutrition. Primary metabolism is fueled with energy and resource which the plant obtain from its environment. Primary metabolites can function as signals in defense pathway. Induced changes in primary metabolism could themselves be defensive. Tolerance depends on primary metabolites and energy. Defenses from secondary metabolism are based on energy and resources from primary metabolism which can be partially resupplied to primary metabolism (Schwachtje and Baldwin 2008). Plant defensive trait is expensive due to energy drain from growth to defensive metabolite production. The expression of defense and tolerance traits requires changes both in primary and secondary metabolism (Schwachtje and Baldwin 2008). Plant pathogen infection leads to changes in secondary metabolism as a plant defense response as well as changes in primary metabolism which affects development of plant (Berger et al., 2007). The plant defense response to control pathogen are associated with increased demands for energy and large carbon flux which are provided by primary metabolism (Bolton 2009).  In infected plant the process governing carbon flow (photosynthesis, respiration and translocation) can be affected. Any change in respiration and translocation of the infected part of the plant can disturb the healthy photosynthetic cells (Sadasivan 1968). The expression of defense and tolerance traits requires changes both in primary and secondary metabolism (Schwachtje and Baldwin 2008).

Primary metabolite in plants are involved in plant defense. The glycolysis, the mitochondrial tricarboxylic acid (TCA) cycle and mitochondrial electron transport are interconnected pathways that generate energy equivalent and carbon skeleton that may be used in the biosynthesis of various metabolites. Glycolysis is a cytosolic pathway that converts glucose to pyruvate resulting in small net gain of ATP (Bolton 2009). The oxidative metabolism of pyruvate by pyruvate dehydrogenase (PDH) forms acetyl-CoA that enters the TCA cycle. TCA cycle is a central metabolic pathway for aerobic processes and is responsible for a major portion of carbohydrate, fatty acid and amino acid oxidation that produces energy and reducing power (Fernie et al., 2004; Araujo et al., 2011).  Electron donors NAD(P)H and FADH2 from primary metabolism pathway can be used in mitochondrial electron transport to produce ATP or be involved directly in various defense pathway such as in reactive oxygen production (Bolton 2009). Phenolics are secondary metabolites required by plant for defense against pathogen (Lattanzio et al., 2006; Caretto et al., 2015). The carbon balance of infected tissues has an impact on plant disease.

A reduction in photosynthetic metabolism and increased cellular demand during resistance response results in increased cell wall invertase activity. This increased cell wall activity cleaves apoplastic sucrose into glucose and fructose. These hexoses are then transported into the cell by hexose transporters where they fulfil the energy and carbon requirement for resistance response. The carbohydrate increase is believed to be metabolic signal that induces defense response (Ehness et al., 1997). Kim et al. (2006) reported that hexokinase regulates the execution of programmed cell death in plant cells, suggesting a link between glucose metabolism and apoptosis.

Inorganic nitrogen is assimilated into the amino acids glutamine, glutamate, asparagine and aspartate, which serves as a nitrogen carriers in plants (Lam et al., 1996)   In response to infection a demand for  carbon will likely shuttle amino acid into energy generating pathways such as TCA  cycle (Bolton 2009). It has also been studied that several pathogenicity genes are controlled by nitrogen starvation (Thomma et al., 2006).

When challenged by pathogen, plant induce several genes associated with primary metabolic pathways including synthesis or degradation of carbohydrates, amino acids and lipids (Rojas et al., 2014).  Wounding of carrot storage root and infection of carrot plants with the bacterial pathogen Erwinia carotovora apoplastic (extracellular or cell wall-bound) invertase was observed (Sturm and Chrispeels 1990). The oxidized lipid molecule has a role in inducible defense response against pathogens either by acting as a deterrant to its growth or as signal involved in induction of defense gene (Dhondt et al., 2001). The switch from housekeeping to defense metabolism results from change in regulatory and signaling circuit and from enhanced demand for energy and biosynthetic capacity in plants to resist pathogen attack (Scheideler et al., 2002). Energy saved from downregulation of primary metabolism is diverted to defense response. The defense signaling cascade mediate by carbohydrate metabolism, photorespiration and amino acid metabolism is negatively regulated when not needed (Rojas et al., 2014).

The phenylpropanoid compounds, often regarded as phytoalexins display antimicrobial properties help plant to fight pathogen attack (Dixon et al., 2002) represent a major flow of carbon from primary metabolism into secondary metabolism (Bolton et al., 2008; Somssich and Hahlbrock 1998).


Araujo, W. L., Nunes-Nesi, A., Nikoloski, Z.,  Sweetlove, L. J. and Fernie, A. R. 2011 Metabolic Control and Regulation of the Tricarboxylic Acid Cycle in Photosynthetic and Heterotrophic Plant Tissues. Plant Cell Environ. 35(1): 1 -21


Berger, S., Sinha, A. K. and Roitsch, T. 2007 Plant Physiology Meets Phytopathology: Plant Primary Metabolism and Plant-Pathogen Interactions. J. Exp. Bot. 58(15-16): 4019 – 4026

doi: 10.1093/jxb/erm298

Bolton, M. D. 2009 Primary Metabolism and Plant Defense—Fuel for the Fire. Mol.Plant Microbe Interact. 22(5): 487 – 497

doi: 10.1094/MPMI-22-5-0487

Bolton, M. D., Kolmer, J. A., Xu, W. W. and Garvin, D. F. 2008 Lr34- Mediated Leaf Rust Resistance in Wheat: Transcript Profiling Reveals a High Energetic Demand Supported by Transient Recruitment of Multiple Metabolic Pathways. Mol. Plant-Microbe Interact. 21(12): 1515 – 1527

doi: 10.1094/MPMI-21-12-1515

Caretto, S., Linsalata, V., Colella, G., Mita, G. and Lattanzio, V. 2015 Carbon Fluxes between Primary Metabolism and Phenolic Pathway in Plant Tissues Under Stress. Int. J. Mol. Sci. 16(11): 26378 – 26394


Dixon, R. A., Achnine, L., Kota, P., Liu, C-J., Reddy, M. S. S. and Wang, L. 2002 The Phenylpropanoid Pathway and Plant Defense-A Genomics Perspective. Mol. Plant Pathol. 3(5): 371 – 390


Dhondt, S., Geoffroy, P., Stelmach, B. A., Legrand, M. and Heitz, T. 2001 Soluble Phospholipase A2 Activity is Induced before Oxylipin Accumulation in Tobacco Mosaic Virus-Infected Tobacco Leaves and is Contributed by Patatin-Like Enzymes. Plant J. 23(4): 431 – 440


Ehness, R., Ecker, M., Godt, D. E. and Roitsch, T. 1997 Glucose and Stress Independently Regulate Source and Sink Metabolism and Defense Mechanisms via Signal Transduction Pathways Involving Protein Phosphorylation. Plant Cell 9(10): 1825 – 1841

doi: 10.1105/tpc.9.10.1825

Fernie, A. R., Carrari, F. and Sweetlove, L. 2004 Respiratory metabolism: Glycolysis, the TCA Cycle and Mitochondrial Electron Transport. Curr. Opin. Plant Biol. 7(3): 254 – 261

doi: 10.1016/j.pbi.2004.03.007

Kim, M., Lim, J-H., Ahn, C. S., Park, K., Kim, G. T., Kim, W. T. and Pai, H-S. 2006 Mitochondria-Associated Hexokinases Play a Role in the Control of Programmed Cell Death in Nicotiana benthamiana[W]. Plant Cell 18(9): 2341 – 2355

doi: 10.1105/tpc.106.041509

Lam, H.-M., Coschigano, K. T., Oliveira, I. C., Melo-Oliveira, R. and Coruzzi, G. M. 1996 The Molecular-Genetics of Nitrogen Assimilation into Amino Acids in Higher Plants. Annu Rev. Plant Physiol. Plant Mol. Biol. 47: 569 – 593


Lattanzio, V., Lattanzio, V. M. T. and Cardinali, A. 2006 Role of Phenolics in the Resistance Mechanisms of Plants against Fungal Pathogens and Insects. Phytochem. Adv. Res. 23 – 67


Rojas, C. M., Senthil-Kumar, M., Tzin, V. and Mysore, K. S. 2014 Regulation of Primary Plant Metabolism during Plant-Pathogen Interactions and its Contribution to Plant Defense. Front. Plant Sci. 5: 17

doi: 10.3389/fpls.2014.00017

Sadasivan, T. S. 1968 Physiology and Plant Pathology. Opening Remark in the Symposium on the: “Impact of Physiology on Plant Pathology” held at Madras on Dec 21 1967 at the 33rd Annual Meeting of the Indian Academy of Sciences. Moir No. 51 from Centre for Advanced Studies in Botany. Page: 95 – 103


Scheideler, M., Schlaich, N. L., Fellenberg, K., Vingron, M., Slusarenko, A. J. and Hoheisel, J. D. 2002 Monitoring the Switch from Housekeeping to Pathogen Defense Metabolism in Arabidopsis thaliana Using cDNA Arrays. J. Biol. Chem.  277(12): 10555 – 10561


Schwachtje, J. and Baldwin, I. T. 2008 Why Does Herbivore Attack Reconfigure Primary Metabolism? Plant Physiol. 146(3): 845 – 851

doi: 10.1104/pp.107.112490

Somssich, I. E. and Hahlbrock, K. 1998 Pathogen Defense in Plants A Paradigm of Biological Complexity. Trends Plant Sci. 3(3): 86 – 90


Sturm, A. and Chrispeels, M. J. 1990 cDNA Cloning of Carrot Extracellular β-Fructosidase and its Expression in Response to Wounding and Bacterial Infection. Plant Cell 2(11): 1107 – 1119


Thomma, B. P. H. J., Bolton, M. D., Clergeot, P-H. and de Wit, P. J. G.  M. 2006 Nitrogen Controls in Planta Expression of Cladosporium fulvum Avr9 but No other Effector Genes. Mol. Plant Pathol. 7(2): 125 – 130

doi: 10.1111/j.1364-3703.2006.00320.x

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out /  Change )

Facebook photo

You are commenting using your Facebook account. Log Out /  Change )

Connecting to %s