PHYTOHORMONE SALICYLIC ACID, JASMONIC ACID AND ETHYLENE AND PLANT DEFENSE RESPONSES (VII)

Plants are capable of differentially activating distinct defense pathways, depending on the inducing signal molecule. Cross-communication between different signal transduction pathways provide regulatory potential for activating multiple resistance mechanisms in varying combinations helping plant to prioritize defense pathway over one another (Reymond and Farmer 1998; Pieterse and van Loon 1999) thereby providing suitable defense against the pathogen encountered. The phytohormone salicylic acid (SA), jasmonic acid (JA) and ethylene (ET) play crucial role in defense signaling. Salicylic acid can activate plant defense against biotrophic and semi-biotrophic pathogens. Systemic acquired resistance (SAR) and induced systemic resistance (ISR) may confer resistance through different pathway. SAR is activated by pathogen attack leading to an increase in SA accumulation resulting in induction of SA-responsive gene expression providing resistance (Delaney et al., 1995; Hunt et al., 1996) and rhizobacteria mediated ISR is controlled by signaling pathway in which JA and ET play a key role (Pieterse et al., 2002). Both SA-dependent and SA-independent pathways are involved in systemic signaling for defense responses (Mauch-Mani and Metraux 1998). The plant growth promoting rhizobacteria (PGPR) can induce systemic resistance that is independent of SA (Pieterse et al., 1996). SA plays a key role in both SAR signaling and disease resistance (Ryals et al., 1996). PR–proteins are induced in response to pathogen attack (Stintzi et al., 1993; vanLoon et al., 1994). It is the major effects of SA in plant defense that induces the expression of pathogenesis-related (PR) genes.

Plant defense is regulated by change in chromatin structure. Chromatin modification can be an important mechanisms to prime plant for enhanced defense (Conrath 2011). Priming follows perception of molecular patterns of microbes or plants, recognition of pathogen-derived effectors or colonisation by beneficial microbes.  Recent study show plant immunity involves regulation by chromatin remodelling and DNA methylation (Luna et al., 2012). Chromatin is a complex of DNA and histones and its condensed structure reduces the accessibility of DNA thus inhibiting transcription. Elevated levels of SA induce changes in chromatin modification around target gene (Iwasaki and Paszkowski 2014). Modification of chromatin can result in local loosening of this structure, creating accessibility of transcriptional machinery and regulatory proteins to the DNA. Changes in gene expression is linked to chromatin remodelling such as histone modifications and histone replacement (van den Burg and Takken 2009). SA can control gene expression by remodelling chromatin at the target genes. Chemical modification of chromatin alter both DNA and histones protein. Histone proteins are subjected to methylation, acetylation, phosphorylation, ubiquitination or sumoylation of histones (Iwasaki and Paszkowski 2014).

 SA participates in the local and systemic response but SAR does not require long-distance translocation of SA. Accumulation of SA during the onset of SAR is preceded by different metabolic signals such as jasmonates (Truman et al., 2007) and indole derived compounds (Truman et al., 2010).  Truman et al. (2007) suggest jasmonates are central to systemic defense acting as the initiating signal for classic SAR. They conclude that jasmonate signaling appears to mediate long-distance information transmission.  Plant signaling molecule SA and JA play a role in induced disease resistance pathways.

NONEXPRESSOR OF PATHOGENESIS-RELATED GENES1 (NPR1) is a regulatory protein.  SAR and ISR both require regulatory protein NPR1 (van Wees et al., 2000).  Spoel et al. (2003) demonstrated NPR1 in crosstalk between the SA- and JA-dependent signaling pathways in plant defense is modulated through the novel function of NPR1 in cytosol. Nuclear localization of NPR1 is essential for SA-mediated defense gene expression and is not required for the suppression of JA signaling, indicating that cross-talk between SA and JA is modulated by the function of NPR1 in the cytosol (Spoel et al., 2003). Kinkema et al. (2000) demonstrated that nuclear localization of NPR1 is essential for its activity in inducing PR genes.

SA could antagonize JA signaling by preventing accessibility of JA-responsive transcriptional regulators to their target genes. This could be achieved by sequestering transcription factors in inactive complexes or by degradation of positive regulators (Caarls et al., 2015). The activation of transcription factor is obstructed by directing transcriptional factor to the cytosol. Furthermore the transcription factors can be kept in check in the nuclear compartment by inducing complex formation with other proteins that inhibit the binding to the DNA, resulting in reduced transcription (Caarls et al., 2015). One possible function for cytosolic NPR1 is that it may sequester JA-regulated transcriptional activators in the cytoplasm, thereby preventing them from moving to the nucleus and activating transcription (Caarls et al., 2015).

Ethylene modulates the allocation of NPR1 function. SA-activated NPR1 functions in nucleus to activate PR genes and in the cytosol to suppress JA-responsive genes. ET signaling allocates more NPR1 to the nucleus to support SA signaling thereby making NPR1 less available in the cytosol for SA-JA cross-talk. In the absence of ET, SA-activated NPR1 monomer may bind a positive regulator of JA-responsive gene expression in the cytosol preventing them from entering the nucleus thus suppression of JA-responsive gene expression. Alternatively NPR1 may activate a negative regulator of JA pathway (Leon-Reyes et al., 2009). ET bypasses the need for NPR1 in SA-JA cross talk, while it enhances NPR1-dependent, SA-responsive PR-1 expression indicating the dual role of NPR1 i.e. in regulating SA-mediated suppression of JA-responsive gene expression  and  SA-mediated activation of  SA-responsive PR gene expression (Leon-Reyes et al., 2009).

Penninckx et al. (1998) conclude that both the ethylene and jsmonate signaling pathways need to be triggered concomitantly and not sequentially to activate plant defensin gene PDF1.2 upon pathogen infection. In this perspective they observed the synergy between ethylene and methyl jasmonate for induction of PDF1.2 in plants. Three alternative model can be conceived for the interaction between ET and jasmonate signals during activation of the PDF1.2 in pathogen challenged Arabidopsis plants (Penninckx et al., 1998):

 Model 1: Pathogen infection initially stimulates synthesis and production of ethylene which subsequently stimulates production of JA which activates expression of PDF1.2.

Model 2: Pathogen infection initially leads to synthesis and production of JA which subsequently triggers elevated production of ethylene which in turn control PDF1.2 expression.

Model 3: Predicts pathogen infection results in simultaneous synthesis and production of ethylene and JA as both are required for induction of expression of PDF1.2 upon pathogen recognition.

Penninckx et al. (1998) found that JA and ET act via parallel pathways to activate the PDF1.2 gene suggests that combinations of JA and ET may have a synergistic effect on the activation of this gene. Cooperation between signaling pathway is controlled by limited signaling molecules providing resistance throughout the plant.

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