Defense in plant are associated with enhanced biological activities including altered translocation and increased synthesis of compounds such as callose, lignin, phytoalexins and nucleic acid. Such increase in biosynthetic activity require energy that must be derived from increased respiratory activity (Smedegaard-Petersen and Tolstrup 1985). Respiration involves breakdown and oxidation of organic compounds, transfer hydrogen (electrons) to molecular oxygen as well as release of utilizable energy within the cell (Hackett 1959). A substantial increase in respiration can be observed in plants infected with biotrophic and necrotrophic pathogen (Walters 2015). An increase in respiration and invertase expression followed by release of hexoses generating signal for activation of plant defense and a decrease in photosynthetic gene expression is observed on attack by pathogen (Berger et al., 2007). Smedegaard-Petersen and Stolen (1981) report that in inoculated, powdery mildew-resistant barley plants there was an increased requirement of host energy due to enhanced biochemical activities involving active defense reactions. The increased respiratory rate deprived the resistant host of energy available for growth although no visible symptom appeared.
Mitochondria is the primary site of adenosine triphosphate (ATP) generation in plant cells, it may also play a role in cell redox homeostasis and signaling (Noctor et al., 2007). The respiratory pathways prevalent throughout nature are glycolysis, the tricarboxylic acid (TCA) and the mitochondrial electron transport chain (Fernie et al., 2004). These interconnected pathways function to generate energy and carbon skeletons that may be used in the biosynthesis of various metabolites. Mitochondria are sites of reactive oxygen species (ROS) production which is believed to contribute to R protein-mediated immune responses (Huang et al., 2013). ROS are constantly produced as a by-product of respiratory chain activity, in addition to their toxic effect they initiate retrograde signaling between the mitochondrion and nucleus (Li et al., 2014). On sensing pathogen mitochondria play a role in the defense strategy, integrating and amplifying different signals such as salicylic acid (SA), nitric oxide, ROS or pathogen elicitors (Colombatti et al., 2014). Mitochondria also produce signal influencing redox state of cells and promote changes in the expression of nuclear gene by mitochondrial retrograde regulation. They may promote programmed cell death in order to avoid progression of pathogen (Colombatti et al., 2014).
Plant glycolysis exist both in the cytosol and plastid and the reactions are catalysed by nuclear-encoded enzymes (Plaxton 1996). Glycolysis is an anaerobic pathway. It oxidizes hexoses to generate ATP, pyruvate and nicotinamide adenine dinucleotide hydrogen (NADH).
The TCA cycle also known as Kreb’s cycle is located in the mitochondrial matrix. The TCA cycle is a crucial component of respiratory metabolism and is composed of eight enzymes present in the mitochondrial matrix. Most of the TCA cycle enzymes are encoded in the nucleus of higher eukaryotes (Schnarrenberger and Martin 2002). Under aerobic condition pyruvate produced by glycolysis can be transported into mitochondria for complete oxidation to CO2 and water. TCA flux may play a role during the set-up of plant defences. The oxidative metabolism of pyruvate by pyruvate dehydrogenase forms acetyl-CoA that enters the TCA cycle. A significant portion of carbon that enters the plant glycolytic and TCA cycle pathway is not oxidized to CO2 but is utilized in the biosynthesis of secondary metabolites, isoprenoids, amino acid, nucleic acid and fatty acid (Plaxton 1996). Balmer et al. (2018) observed that citrate and fumarate of the TCA cycle induce priming in Arabidopsis against bacterial pathogen. Both citrate and fumarate show no antibacterial effect and therefore resistance in plant is due to the induction of plant defense system.
Oxidative phosphorylation (ATP synthesis). The NADH is used by the electron chain complexes to generate a proton gradient across the inner mitochondrial membrane. The electrochemical potential across the inner membrane is the force that drives the synthesis of ATP (Lodish et al., 2000; Millar et al., 2011). Barley leaves when infected with powdery mildew showed increased respiration rate. The increase is due to increased electron flow through cytochrome chain through alternative pathway (Farrar and Rayns 1987).
SA effects electron transport and oxidative phosphorylation of plant mitochondria (Xie and Chen 1999). SA induce alternative pathway respiration by activating expression of the alternative oxidase gene. Xie and Chen (1999) report rapid mode of action by SA on plant mitochondrial functions. SA induced inhibition of ATP synthesis and respiratory oxygen uptake may also play a role in the involvement of SA in pathogen-induced hypersensitive response. Inhibition of mitochondrial function by SA may play a role in plant defense responses.
The degradation of fatty acid during β-oxidation is another potential energy source during plant defense (Bolton 2009). Glycolysis, the TCA and β-oxidation of fatty acid were induced in the alfalfa leaves at later stages of Phoma medicaginis infection (Fan et al., 2018). Intermediates metabolites and some amino acids metabolic pathway like glycine, leucine, isoleucine, tyrosine and lysine accumulated at an early stage of infection enabling the plant to resist necrotrophic Phoma medicaginis. Palmitic acid and stearic acid accumulation at early infection stages may enhance plant resistance (Fan et al., 2018). In hypoxic condition pyruvate can be broken down by lactate dehydrogenase to form lactate and NAD. This serves purpose for energy production, the anaerobic regeneration of NAD for glycolysis (Bolton 2009). Metabolic pathway indicate photosynthesis and respiration are important components of the plant response to infection.
References:
Balmer, A., Pastor, V., Glauser, G. and Mauch-Mani, B. 2018 Tricarboxylates Induce Defense Priming against Bacteria in Arabidopsis thaliana. Front. Plant Sci. 9: 1221
doi: 10.3389/fpls.2018.01221
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. MPMI 22(5): 487 – 497
doi: 10.1094/MPMI-22-5-0487
Colombatti, F., Gonzalez, D. H. and Welchen, E. 2014 Plant Mitochondrion under Pathogen Attack: A Sigh of Relief or a Last Breath? Mitochondrion 19(B): 238 – 244
doi.org/10.1016/j.mito.2014.03.006
Fan, Q., Creamer, R. and Li, Y. 2018 Time-Course Metabolic Profiling in Alfalfa Leaves under Phoma medicaginis infection. PLoS ONE 13(10): e0206641
doi.org/10.1371/journal.pone.0206641
Farrar, J. F. and Rayns, F. W. 1987 Respiration of Leaves of Barley Infected with Powdery Mildew: Increased Engagement of the Alternative Oxidase. New Phytol. 107(1): 119 – 125
doi.org/10.1111/j.1469-8137.1987.tb04886.x
Fernie, A. R., Carrari, F. and Sweetlove, L. J. 2004 Respiratory Metabolism: Glycolysis, the TCA Cycle and Mitochondrial Electron Transport. Curr. Opin. Plant Biol. 7(3): 254 – 261
doi.org/10.1016/j.pbi.2004.03.007
Hackett, D. P. 1959 Respiratory Mechanisms in Higher Plants. Annu. Rev. Plant Physiol. 10: 113 – 146
annualreviews.org/doi/pdf/10.1146/annurev.pp.10.060159.000553
Huang, Y., Chen, X., Liu, Y., Roth, C., Copeland, C., McFarlane, H. E., Huang, S., Lipka, V., Wiermer, M. and Li, X. 2013 Mitochondrial AtPAM16 is required for Plant Survival and the Negative Regulation of Plant Immunity. Nat. Commun. 4: 2558
doi.org/10.1038/ncomms3558
Li, Z., Liang, W-S. and Carr, J. P. 2014 Effects of Modifying Alternative Respiration on Nitric Oxide-Induced Virus Resistance and PR1 Protein Accumulation. Journal of General Virology 95: 2075 – 2081
doi: 10.1099/vir.0.066662-0
Lodish, H., Berk, A., Zipursky, S. L., Matsudaira, P., Baltimore, D. and Darnell, J. 2000 Electron Transport and Oxidative Phosphorylation. In “Molecular Cell Biology 4th Edition”. Freeman, W. H. (ed.). New York. Section 16.2
http://www.ncbi.nlm.nih.gov/books/NBK21528/
Millar, A. H., Whelan, J., Soole, K. L. and Day, D. A. 2011 Organization and Regulation of Mitochondrial Respiration in plants. Annu. Rev. Plant Biol. 62: 79 – 104
doi: 10.1146/annurev-arplant-042110-103857
Noctor, G., De Paepe, R. and Foyer, C. H. 2007 Mitochondrial Redox Biology and Homeostasis in Plants. Trends Plant Sci. 12(3): 125 – 134
doi: 10.1016/j.tplants.2007.01.005
Plaxton, W. C. 1996 The Organization and Regulation of Plant Glycolysis. Annu. Rev. Plant Physiol. Plant Mol. Biol. 47: 185 – 214
doi.org/10.1146/annurev.arplant.47.1.185
Schnarrenberger, C. and Martin, W. 2002 Evolution of the Enzymes of the Citric Acid Cycle and the Glyoxylate Cycle of Higher Plants. A Case Study of Endosymbiotic Gene Transfer. Eur. J. Biochem. 269(3): 868 – 883
doi: 10.1046/j.0014-2956.2001.02722.x
Smedegaard-Petersen, V. and Stolen, O. 1981 Effect of Energy-Requiring Defense Reactions on Yield and Grain Quality in a Powdery Mildew-Resistant Barley Cultivar. Phytopathology 71(4): 396 – 399
doi: 10.1094/Phyto-71-396
Smedegaard-Petersen, V. and Tolstrup, K. 1985 The Limiting Effect of Disease resistance on Yield. Ann. Rev. Phytopathol. 23: 475 – 490
doi.org/10.1146/annurev.py.23.090185.002355
Walters, D. R. 2015 Respiration in Plants Interacting with Pathogens, Pests and Parasitic Plants. In “Physiological Responses of Plants to Attack”. Chapter 4: 88- 113
doi.org/10.1002/9781118783054.ch4
Xie, Z. and Chen, Z. 1999 Salicylic Acid Induces Rapid Inhibition of Mitochondrial Electron Transport and Oxidative Phosphorylation in Tobacco Cells. Plant Physiol. 120: 217 – 225
doi.org/10.1104/pp.120.1.217
BIOLOGICAL PROCESSES- A NATURE'S GIFT 