Plant can sense invading pathogen through recognition of either conserved pathogen or microbe- associated molecular patterns (PAMPS/MAMPS) or pathogen derived effectors. The highly conserved PAMPs (or MAMPs) is recognized by transmembrane proteins that function as pattern recognition receptor (PRRs) which in turn activates PAMPs-triggered immunity (PTI) through various signal transduction pathway leading to defense responses. Some pathogens secrete effectors into the host cells to suppress PTI. The R-genes present in plant encode proteins which can recognize avirulent (Avr) pathogen proteins (effectors), initiating defense responses leading to hypersensitive response (Chisholm et al., 2006; Jones and Dangl 2006).

Plants have both constitutive and inducible barriers for defense against pathogen attack. Some inducible defences depends on action of phytohormone salicylic acid, ethylene and jasmonate (Feys and Parker 2000; McDowell and Dangl 2000; Gimenez-Ibanez and Solano 2013). Salicylic acid (SA) induce resistance against biotrophic pathogen whereas, jasmonic acid (JA) and ethylene (ET) induce resistance against necrotrophic pathogen (Glazebrook 2005). Systemic acquired resistance (SAR) is an induced defense mechanisms that confers protection against wide range of pathogens. SAR requires signal molecule SA and is associated with de-novo synthesis of pathogenesis-related (PR) protein which may affect pathogen growth and proliferation. In response to SA, the positive NONEXPRESSOR OF PR GENES1 (NPR1) moves to the nucleus where it interacts with TGA transcription factors to induce defense gene expression, activating SAR (Durrant and Dong 2004).   SA, JA and ET signaling depends on the sequence of initiation in which these plant hormones are produced (Leon-Reyes et al., 2010):

  • If  SA pathway is activated prior to or at the same time as JA pathway, then SA pathway will suppress JA response 
  • If JA pathway is activated first in the absence of ethylene, then SA can still suppress the JA response and
  • If  JA and ET pathways are activated simultaneously then the JA/ET response becomes insensitive to suppression by SA

Cross talk between induced signaling pathways can provide plant with regulatory potential. Signaling interaction can be synergistic or mutually antagonistic (Koornneef and Pieterse 2008). van Wees et al. (2000) reported SA-dependent systemic acquired resistance (SAR) pathway and JA-dependent induced systemic resistance (ISR) pathway can occur concurrently without any significant cross talk between these pathways. SAR and ISR both require the regulatory protein NPR1 and that constitutive level of NPR1 is sufficient to facilitate simultaneous expression of SAR and ISR.

Plant can mount an appropriate immune response against pathogen that stimulates biosynthesis of SA, JA and ET.   Antagonistic effect of SA on JA signaling requires NPR1 (Spoel et al., 2003, Thaler et al., 2012). Nuclear localization of NPR1 is essential for SA mediated defense gene expression, however, it is not required for suppression of JA signaling, indicating that cross-talk between SA and JA is regulated by NPR1 in the cytosol (Spoel et al., 2003).  NPR1 may directly interferes with JA signaling or indirectly interfere through the transcriptional factor genes and/or glutaredoxin genes which can be implicated in SA-JA crosstalk. The SA-activated NPR1 induces glutaredoxin which in turn interacts with TGA transcription factors to suppress JA-responsive gene (Koornneef and Pieterse 2008).

  • Plants when attacked by the biotrophic pathogen results in accumulation of salicylic acid  bringing in SA-mediated redox change followed by monomerization of  NPR1 in the cell. Monomeric NPR1 is then translocated into the nucleus where it interacts with TGA transcription factors (regulators of pathogenesis-related gene), leading to activation of SA-responsive genes. Expression of large set of WRKY genes is induced by SA some of which can regulate SA-responsive gene expression (Van der Does et al., 2013). Example production of PR-1 proteins. Plant specific transcription factor WRKY70 is common component in SA and JA mediated signal pathway. Expression of WRKY70 is activated by SA and repressed by JA. High WRKY70 level activates expression of SAR-related genes while repressing JA-responses over SAR. (Li et al., 2004).
  • Plants when attacked by necrotrophic pathogen results in accumulation of jasmonic acid (JA). The binding of JA to E3 ubiquitin-ligase complex SCFCOI1 [CORONATINE INSENSITIVE1 (COI1) functions as a jasmonate receptor (a key regulator of JA signaling) and forms skp1/Cullin1/F-box protein COI1 (SCFCOI1)] leads to degradation of JASMONATE ZIM-domain transcriptional repressor proteins (JAZs) via the proteasome, resulting in the release of transcriptional activator. Subsequently transcription factors APETALA2/ETHYLENE RESPONSE FACTOR (AP2/ERF) like OCTA-DECANOID-RESPONSIVE ARABIDOPSIS AP2/ERF domain protein 59 (ORA59)  and ETHYLENE RESPONSE FACTOR1 (ERF1) are induced  which activates the ERF of the JA pathway (Van der Does et al., 2013). Binding of ERFs (ORA59) to the GCC-box induces JA-responsive gene expression, which can be suppressed by SA in an SCFCOI1-JAZ –independent manner. The GCC-box is sufficient for SA-mediated suppression of JA-induced gene expression. Salicylic acid can negatively affect ORA59 protein accumulation which explains the antagonistic effect of SA on JA responsive gene expression (Van der Does et al., 2013).

Ethylene is known to enhance SA/NPR1-dependent defense responses. Leon-Reyes et al. (2009) suggested ET modulates the NPR1 dependency of SA-JA antagonism possibly to enhance NPR1 to function in SA-dependent activation of PR genes. ET modulates the positive and negative functions of NPR1. SA-activated NPR1 functions in the nucleus to activate PR genes and acts in cytosol to suppress JA-responsive genes. ET signaling allocates more NPR1 to the nucleus to support SA signaling whereas, it makes less NPR1 available in the cytosol for SA-JA cross talk.  In absence of ethylene, SA-activated NPR1 monomers may bind a positive regulator of JA responsive gene expression in cytosol which is then prevented from entering the nucleus, resulting in the suppression of JA-responsive gene expression (Leon-Reyes et al., 2009). In general ERF is associated with enhanced resistance to necrotroph. Depending on the type of pathogen, ERF1 can be activated by ethylene or jasmonate or synergistically by both signaling pathways. Lorenzo et al. (2003) suggest that ERF1 transcription factor is the main element in the integration of both signals for regulation of defense response genes. 


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doi: 10.3389/fpls.2013.00072

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


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


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Leon-Reyes, A., Du, Y., Koornneef, A., Proitti, S., Korbes, A. P., Memelink, J., Pieterse, C. M. J. and Ritsema, T. 2010  Ethylene Signaling Renders the Jasmonate  Response of Arabidopsis Insensitive to Future Suppression by Salicylic Acid. MPMI 23(2): 187 – 197


Lorenzo, O., Piqueras, R., Sanchez-Serrano, J. J. and Solano, R. 2003 ETHYLENE RESPONSE FACTOR1 Integrates Signals from Ethylene and Jasmonate Pathways in Plant Defense. Plant Cell 15(1): 165 – 178


Li, J., Brader, G. and Palva, E. T. 2004 The WRKY70 Transcription Factor: A Node of Convergence for Jasmonate-Mediated and Salicylate-Mediated Signals in Plant Defense. Plant Cell 16: 319 – 331


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