Plant have a pathogen-recognition system to balance the absence of adaptive or specific immune system. Plant immune system comprises of two tier of receptor. One sensing molecule outside the cell and the other sensing molecule inside the cell. Both system sense the invader and respond to the pathogen and related pathogenesis event. The cell surface pattern recognition receptors (PRRs) senses microbial signature and intracellular nucleotide binding domain leucine-rich repeat (NLR)   recognizes pathogen effector (Mang et al., 2017;   Noman et al., 2019). The first tier which is plasma-membrane- localized PRRs that recognizes pathogen- or microbe- or damage associated molecular patterns (PAMPs/ MAMPs/ DAMPs) can be categorized as plasma-membrane-localized receptor kinases (RKs) or receptor-like proteins (RLPs). PAMPs recognition signaling events activate pathogen related responses such as increase in cytosolic Ca2+, reactive oxygen species (ROS) production and kinase activation, protein phosphorylation and variation in gene regulation for production of antimicrobial compound (Noman et al., 2019). The system is known as PAMPs triggered immunity (PTI). The second tier primarily is governed by resistance (R) protein that recognize effector (Avr gene protein) and activate effector- triggered immunity (ETI) in a gene–for-gene mode (Martin et al., 2003). Cytosolic recognition of pathogenic effectors by nucleotide-binding and leucine-rich-repeat (NB-LRR) proteins activates ETI resulting into hypersensitive response (Mesarich et al., 2018) that prevents further infection. Pathogen triggered immunity and ETI may be mediated by salicylic acid (SA), jasmonic acid (JA) and ethylene (ET) dependent signaling mechanisms (Lai et al., 2013). The plant pathogen use effector to inhibit PRR complexes (Boller and Felix 2009) thus PTI is suppressed by the effector proteins.  

Plant hormones like JA, SA and ET are primarily involved in plant defense while abscisic acid (ABA), Auxins [Indole-3-acetic acid (IAA)], Cytokinins (CKs), Brassinosteroids (BRs), Gibberellins (GAs) and Strigolactones (STR) regulate plant defense (Robert-Seilaniantz et al., 2011) either alone or in conjunction with the primary defense hormone. SA, JA, ET, ABA, GA, CK and BR all are implicated in plant defense signaling pathway (Bari and Jones 2009). Pathogens have developed strategies via their effector repertoire to either interfere or hijack phytohormone pathway to induce resistance or susceptibility (Kazan and Lyons 2014). Plant hormones interact in complex manner governing plant immunity. The hormone signaling pathway are targeted by pathogens to evade plant defense responses (Denance et al., 2013).

It has been demonstrated that the salicylic acid (SA)-dependent pathway is mostly involved in defense against biotrophic pathogens, while jasmonic acid (JA) and ethylene (ET) signaling pathways are mainly associated with defense against necrotrophic pathogens  (Glazebrook 2005). Both PTI and ETI are modulated by plant hormone SA, JA and ethylene (Bajguz and Hayat 2009). ABA can act as both a positive and a negative regulator of disease resistance by interacting with SA-JA-ET of the plant immune system (Asselbergh et al., 2008). Denance et al. (2013) studied the regulatory roles of the ABA, SA and auxin in plant resistance to pathogens:


Abscisic acid is an isoprenoid compound that regulates developmental processes such as seed development, dessication and dormancy (Wasilewska et al., 2008). ABA has emerged as a complex modulator of plant defense responses and involves a crosstalk with SA or ethylene/JA-associated signaling pathways. Fan et al. (2009) reported that physiological level of ABA play an important role in modulating diverse plant-pathogen interactions and elaborate a link between abiotic stress and level of disease susceptibility. ABA can influence resistance against both necrotrophs and biotrophs positively and negatively (Asselberg et al., 2008). The antagonistic or synergistic interaction between abiotic and biotic stress responses indicate that ABA is an essential component in integrating and fine tuning biotic stress response signaling network (Asselberg et al., 2008).  Abscisic acid and ethylene can act synergistically with   JA-regulated responses while generally antagonizing SA responses (Caarls et al., 2015). Calcium sensors decode the nature of the stimuli and the signals are then transduced through appropriate hormone pathway to bring series of physiological responses (Ku et al., 2018). Abscisic acid and JA coordinate with Ca2+ signal. Therefore it is assumed that ABA and JA are the convergent point between abiotic and biotic stresses. Ca2+ sensor acts as both a stress signal detector and as a regulator of ABA and JA signaling.

ABA regulates stomatal closure which is important for pathogen control   (Lim et al., 2015). ROS are important messengers in ABA mediated stress responses. ABA signaling in guard cell require ROS formation to interact with Ca+ channels to induce stomatal closure (Kwak et al., 2003; Li et al., 2006). Various plant hormone pathways crosstalk with one another and switch responses from one pathway to another.

                                                               See Part II for further information

                                                                                         Continue ……………


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Bari, R. and Jones, J. D. G.  2009 Role of Plant Hormone in Plant Defense Responses. Plant Mol. Biol. 69(4): 473 – 488


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Denance, N., Sanchez-Vallet, A., Goffner, D. and Molina, A. 2013 Disease Resistance or Growth: The Role of Plant Hormones in Balancing Immune Responses and Fitness Costs. Front. Plant Sci. 24 May

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Li, S., Assmann, S. M. and Albert, R. 2006 Predicting Essential Components of Signal Transduction Networks: A Dynamic Model of Guard Cell Abscisic Acid Signaling. PLoS Biol.  4(10): e312

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Mang, H., Feng, B., Hu, Z., Boisson-Dernier, A., Franck, C. M., Meng, X., Huang, Y., Zhou, J., Xu, G., Wang, T., Shan, L. and He, P. 2017 Differential Regulation of Two-Tiered Plant Immunity and Sexual Reproduction by ANXUR Receptor-Like Kinases. Plant Cell 29(12): 3140 – 3156

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Martin, G. B., Bogdanove, A. J. and Sessa, G. 2003 Understanding the Functions of Plant Disease Resistance Proteins. Annu. Rev. Plant Biol. 54: 23 – 61


Mesarich, C. H., Okmen, B., Rovenich, H., Griffiths, S. A., Wang, C., Karimi Jashni, M., Mihajlovski, A., Collemare, J., Hunziker, L., Deng, C. H., van der Burgt, A., Beenen, H. G., Templeton, M. D., Bradshaw, R. E. and de Wit, P. J. G. M. 2018 Specific Hypersensitive Response-Associated Recognition of New Apoplastic Effectors from Cladosporium fulvum in Wild Tomato.   Mol. Plant Microbe Interact. 31(1): 145 – 162

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Noman, A., Aqeel, M. and Lou, Y. 2019 PRRs and NB-LRRs: From Signal Perception to Activation of Plant Innate Immunity. Int. J. Mol. Sci. 20(8): 1882


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Wasilewska, A., Vlad, F., Sirichandra, C., Redko, Y., Jammes, F., Valon, C., Frei dit Frey, N. and Leung, J. 2008 An Update on Abscisic Acid Signaling in Plants and More. Mol. Plant 1(2): 198 – 217

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