Plant must cope with the changing environment as some of the conditions may impose severe stress. Hence sensing and responding to biotic/abiotic stress is to ensure survival. A major challenge to plant is to distinguish pathogens from commensal or beneficial microorganisms and activate defense response against the pathogen attack. Plant employs several cell surface and intracellular immune receptor to perceive different immunogenic signals associated with pathogen attack and activate defense response against the invading pathogen (Zhou and Zhang 2020). Systemic acquired resistance (SAR) is activated upon local infection (Klessig et al., 2018). The activation of local defense response leads to secondary immune response in distal uninfected tissue is known as systemic acquired resistance (SAR). Long distance signaling involves many SAR-inducing chemicals that include salicylic acid (SA), methyl salicylic acid (MeSA), azelic acid (AzA), glycerol-3-phosphate (G3P), dehydroabietinal, pipecolic acid (Pip), N-hydroxypipecolic acid (NHP), the free radicals nitric oxide (NO), reactive oxygen species (ROS) and galactolipids (Lim 2023). During pathogen infection SA is synthesized in cytoplast and is transported via apoplast, whereas AzA and G3P are transported by symplastic transport through plasmodesmata (Lim et al., 2016). NHP is synthesized from Pip. Pip is transported to cytosol where it is converted to NHP via cytosol localized flavin-dependent monooxygenase1 (FMO1) (Hartmann et al., 2018). SAR an immune response is established in the systemic leaves after being infected with biotrophic or hemibiotrophic pathogens. The NHP travel from the infected site to the distal uninfected leaves where it induces the biosynthesis of SA resulting in robust SAR response (Nair 2021).
SA, NHP and its precursor pipecolic acid plays a role in plant immune signaling and is required for SAR (Navarova et al., 2012). SA an endogenous defense signal can induce systemic acquired resistance in plant (Gaffney et al., 1993). The NHP metabolite are mobile defense signal produced at the site of bacterial infection and establish defense in healthy distal tissues (SAR) (Chen et al., 2018). Hence both SA and N-hydroxypipecolic acid are two major chemical signals that control SAR (Honig et al., 2023). NHP in SAR can directly induce SAR gene expression, signal amplification, priming for enhanced defense activation and with SA signaling may ensure enhanced plant immunity (Hartmann and Zeier 2019). Upon SAR induction via SA and/or NHP activation of NPR1(nonexpresser of pathogenesis-related genes1) protein must occur inducing PR gene expression and resistance to infection (Cao et al.,1997). SA binds to NPR1 to induce SAR gene expression while perception of NHP still needs to be elucidated (Guerra and Romeis 2020). Despite structural similarity between SA and NHP, the NHP did not bind to NPR1 in vitro while SA bound to NPRI with a Kd value of 585 + 368 nM (Nair 2021). NHP primes plant involving SAR in both SA-dependent and SA-independent pathway (Bernsdorff et al., 2016).
SA is perceived by two classes of receptors. NPR1 and paralogues NPR3 and NPR4 are SA receptors that bind SA with different affinities. NPR3 and NPR4 function as an adaptor of the Cullin 3 ubiquitin E3 ligase to mediate NPR1 degradation in a SA-regulated manner (Fu et al., 2012). NPR1 functions as transcriptional co-activator, whereas NPR3/NPR4 functions as E3 ligases that mediate NPR1 degradation. Binding of SA to NPR3/NPR4 inhibits the transcriptional repression activity, and the perception of SA by NPR1 promotes the transcriptional activation activity, both contribute to induction of defense gene expression (Ding et al., 2018). When there is low SA level, NPR3/NPR4 repress defense gene expression, which prevents autoimmunity. Increased SA accumulation removes the repression and allows the induction of defense gene expression through the transcription coactivator NPR1(Ding et al., 2018). The perception of SA by NPR1 and NPR4 is required for activation N-hydroxypipecolic acid biosynthesis which is essential for inducing SAR (Liu et al., 2020). In distal tissues, NHP promotes SA biosynthesis and SA-induced resistance (Liu et al., 2020).
The non-SA SAR pathway is driven by Pip or its bioactive derivative NHP (Vlot et al., 2021). This pathway regulates inter-plant defense propagation through volatile organic compound emitted by SAR-induced plant recognized as defense cues by the neighbouring plants (Vlot et al., 2021). Both SAR and ISR (induced systemic resistance) influence phytohormone crosstalk. Jasmonic acid (JA) and ethylene (ET) but also a synergism of JA and SA signaling (Vlot et al., 2021) have a role in interaction of plant with beneficial plant growth promoting rhizobacteria (PGPR) and plant growth promoting fungi (PGRF) providing effective plant protection. Plant root associated PGPR/PGPF induce ISR which primes plant against necrotrophic pathogens (Conrath et al., 2002) and improves plant resistance against (hemi-)biotrophic pathogen (Vlot et al., 2021). The rhizobacteria-mediated ISR requires responsiveness to JA and ET and is dependent on NPR1 (Pieterse et al., 1998). SAR, NPR1 functions as a transcriptional coactivator of SA-responsive PR genes; rhizobacteria-mediated ISR functions without PR genes activation (Pieterse et al., 2014). NPR1, NPR3 and NPR4 genes are highly expressed in Arabidopsis root suggesting a role in regulation of root associated immune responses (Pieterse et al., 2014).
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