PLANT DEFENSE RESPONSES

Plants are sedantry autotroph, lack circulatory system but they have innate immune system that is activated after recognition of the pathogen. Plant respond to infection using two branch of innate immune system. One branch recognize and respond to molecule common to microbe including non-pathogen while the second respond to pathogens virulence factor directly affecting the host target (Jones and Dangl 2006).

  1. Plants are provided by pattern recognition receptors (PRRs) that are receptor kinases or receptor proteins which recognizes pathogen-associated molecular patterns or microbe-associated molecular patterns (PAMPs or MAMPs) and play a significant role in immune signaling (Boller and Felix 2009;  Li et al., 2016;  Saijo et al., 2018) leading to activation of defense responses.  

Disease develop when pathogens are able to evade or suppress PRR-based defenses. Pathogens escape from being recognized by the host’s immune system is due to modification in the structure of the recognized MAMPs or by active intervention of ligands-receptor recognition (Pel and Pieterse 2012).    

Plant cells close their plasmodesmata during pathogen infection.  Plasmodesmata (PD) is plasma membrane lined pore that connects the adjoining cells maintaining the continuity of cytoplasm and endomembrane. Proteins, metabolites, small RNAs and hormones are transported through these PD during defense signaling.  Systemic defense responses depend on the spread of signals between cells. Plasmodesmata is regulated by callose deposition. Deposition of β-1,3-glucan callose in the apoplast around PD reduces the aperture of the pore. In this manner symplastic connection can be opened or closed (Tilsner 2016; Cheval and Faulkner 2018). 

Some PRRs can recognize damage-associated molecular patterns (DAMPs) that are plant derived molecule released during pathogen infection. Phytopathogens secrete effectors into plants apoplast or cytoplasm to enhance virulence (Li et al., 2016). Signal is transmitted through a cell and across the cell membranes as a series of events and relies on proteins known as receptors. It is these receptors that perceive signals for regulation of plant immunity.

2. Plant disease resistance involves a single resistance (R) gene in the plant which responds specifically to an avirulence (Avr) gene (gene for-gene concept). R genes encode proteins that appear to be involved in both recognition of the pathogen and signal transduction (Halterman and Martin 1997). The interaction of pathogen effector (Avr gene protein) with the host receptors (many of which may be encoded by R genes) generates the initial recognition signal that triggers activation of signal transduction pathway culminating in activation of the defence response resulting in a localised cell death at the site of infection termed as hypersensitive response (HR) which prevents the further spread of the infection. Plant use wide range of defense mechanisms to defend themselves such as generation of active oxygen species (AOS),   cell wall strengthening, deposition of callose, accumulation of pathogenesis-related (PR) proteins and phytoalexin (Hammond-Kosack and Jones 1996; Halterman and Martin 1997; Van Loon and Van Strien 1999). Massive accumulation of reactive oxygen species (ROS) and salicylic acid (SA) is also reported by Guidetti-Gonzalez et al. (2007).

Microbial elicitors causes rapid production of reactive oxygen intermediate.  The active oxygen species (AOS) are toxic intermediates such as superoxide anion (O2), hydrogen peroxide (H2O2) and hydroxyl radical (OH). The oxidative burst is correlated with the HR in many plant-pathogen interactions contributing to disease resistance (Mehdy 1994). H2O2 is more stable hence can diffuse across membranes, whereas, OH cannot migrate and therefore reacts locally. H2O2 and OH can react with polyunsaturated lipids in membrane forming lipid peroxide which can lead to disruption of biological membrane (Grant and Loake 2000). As the cells are unable to detoxify OH, an excess molecule can lead to cell death.

Levine et al. (1994) reported that H2O2 from oxidative burst drives cross-linking of cell wall structural proteins as well as play a key role in localized hypersensitive response. H2O2 also function as a diffusible signal, inducing cellular protectants such as glutathione S-transferase and glutathione peroxidase. Chen et al. (1993) studied, salicylic acid inhibited catalase activity inducing the increased production of H2O2. The action of salicylic acid in systemic acquired resistance is mediated by elevated amount of H2O2.  Increased H2O2 concentration resulting from catalase inhibition serves as a second messenger in the transcriptional activation of pathogenesis-related protein genes (Mehdy 1994).

HR is associated with plant resistance to pathogen infection (Morel and Dang 1997). On detection of activation of HR, the uninfected part of the plant may develop resistance to control the further spread of infection by phenomena known as systemic acquired resistance (SAR). Durner et al. (1997) reported salicylic acid to be a signaling molecule and is involved in local defense reaction at the infection site and induction of systemic resistance. The systemic acquired resistance (SAR) confers a broad-based resistance against different pathogens (Ryals et al., 1996; Delaney 1997).

Plants can activate separate defense pathways depending on the type of pathogen encountered (Garcia-Brugger et. al., 2006). Jasmonic acid (JA) and ethylene dependent responses seem to be initiated by necrotrophs whereas, salicylic acid (SA) dependent response is activated by biotrophic pathogens (Glazebrook 2005). The two major defense signaling pathway are:

  • SA-dependent pathway 
  • SA-independent pathway that involves Jasmonic Acid (JA) and ethylene

These pathways do not function independently. The crosstalk among JA, ethylene and SA signaling pathways is through complex network of regulatory interactions (Kunkel and Brooks 2002).  

A resistant plant is capable of prompt recognition of the pathogen and activates the defense responses rapidly and effectively. Whereas, a susceptible plant exhibits weaker and a slower response. 

References:

Boller, T. and Felix, G. 2009 A Renaissance of Elicitors: Perception of Microbe-Associated Molecular Pattern and Danger Signals by Pattern-Recognition Receptors. Annu. Rev. Plant Biol. 60: 379 – 406

doi: 10.1146/annurev.arplant.57.032905.105346

Chen, Z., Silva, H. and Klessig, D. F. 1993 Active Oxygen Species in the Induction of Plant Systemic Acquired Resistance by Salicylic Acid. Science 262(5141): 1883 – 1886

doi: 10.1126/science.8266079

Cheval, C. and Faulkner, C. 2018 Plasmodesmal Regulation during Plant-Pathogen Interactions. New Phytol. 217(1): 62 – 67

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Delaney, T. P.  1997 Genetic Dissection of Acquired Resistance to Disease. Plant Physiol. 113 (1): 5-12

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Durner, J., Shah, J. and   Klessig, D. F. 1997 Salicylic Acid and Disease Resistance in Plants. Trends Plant Sci. 2(7): 266-274

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Garcia-Brugger, A.,   Lamotte, O.,   Vandelle, E.,  Bourque, S.,  Lecourleux, D., Poinssot, B., Wendehenne, D. and Pugin, A. 2006 Early Signalling Events Induced by Elicitors of Plant Defences. MPMI   19 (7): 711–724

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Glazebrook, J. 2005 Contrasting Mechanisms of Defense against Biotrophic and Necrotrophic Pathogens. Annu. Rev. Phytopathol. 43: 205-227

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Grant, J. J. and Loake, G. J. 2000 Role of Reactive Oxygen Intermediates and Cognate Redox Signaling in Disease Resistance. Plant Physiol. 124: 21-30

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Guidetti-Gonzalez, S., Freitas-Astua, J., Morais do Amaral, A., Martins, N. F.,  Mehta, A., Silva, M. S. and  Carrer, H. 2007 Genes Associated with Hypersensitive Response (HR) in the Citrus EST Database (CitEST). Genet. Mol. Biol. 30(3) Suppl.,  pp. 943-956

doi.org/10.1590/S1415-47572007000500022

Halterman, D. A. and Martin, G. B. 1997 Signal Recognition and Transduction Involved in Plant Disease Resistance. Essays Biochem. 32: 87 – 99

https://www.ncbi.nlm.nih.gov/pubmed/9493013

Hammond-Kosack, K. E.  and   Jones, J. D. G.  1996   Resistance Gene-Dependent Plant Defense Responses.  Plant Cell 8(10): 1773-1791

doi.org/10.1105/tpc.8.10.1773

Jones, J. D. G. and Dangl, J. L. 2006 The Plant Immune System. Nature 444(7117): 323 – 329

doi:10.1038/nature05286

Kunkel, B. N. and Brooks, D. M. 2002 Cross Talk between Signaling Pathways in Pathogen Defense. Curr. Opin. Plant Biol. 5: 325-331

doi 10.1016/S1369-5266(02)00275-3

Levine, A., Tenhaken, R., Dixon, R. and Lamb, C. 1994 H2O2 from the Oxidative Burst Orchestrates the Plant Hypersensitive Disease Resistance Response. Cell 79(4): 583 – 593

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Li, L., Yu, Y., Zhou, Z. and Zhou, J. M. 2016 Plant Pattern-recognition Receptors Controlling Innate Immunity. Sci. China Life Sci. 59(9):  878–888

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Mehdy, M. C. 1994 Active Oxygen Species in Plant Defense against Pathogens. Plant Physiol. 105: 467 – 472

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Morel, J. B. and Dangl, J. L. 1997 The Hypersensitive Response and the Induction of Cell Death in Plants. Cell Death Differ. 4(8): 671 – 683

doi:10.1038/sj.cdd.4400309

Pel, M. J. C. and Pieterse C. M. J. 2013 Microbial Recognition and Evasion of Host Immunity.  Journal of Experimental Botany 64(5):  1237–1248

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Ryals, J. A., Neuenschwander, U. H., Willits, M. G., Molina, A., Steiner, H. Y. and Hunt, M. D.  1996  Systemic Acquired Resistance. Plant Cell 8(10): 1809-1819

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Saijo, Y., Loo, E. P. and Yasuda, S. 2018 Pattern Recognition Receptors and Signalling in Plant-Microbe Interactions. Plant J. 93(4): 592 – 613

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Tilsner, J., Nicolas, W., Rosado, A. and Bayer, E. M. 2016 Staying Tight: Plasmodesmal Membrane Contact Sites and the Control of Cell-to-Cell Connectivity in Plants. Annu. Rev. Plant Biol..  67: 337-364

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Van Loon, L. C.  and Van Strien, E. A. 1999 The Families of Pathogenesis-related Proteins, their Activities, and Comparative Analysis of PR-1 type Proteins.  Physiological and Molecular Plant Pathology   55(2): 85–97

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