The plant immune system
Co-habitation of plants and microbes has engaged them into the evolution of a diverse range of strategies to attack each other or defend themselves from one another. Plant pathogens employ various molecules to impair plant growth and reproduction. Unlike animals, plants do not have a specialized somatic mobile immune system. Therefore, plants have developed interconnected innate immune responses that recognize and respond to pathogen infections. The plant immune system consists of two branches: PAMP-triggered immunity (PTI) and effector-triggered immunity (ETI).
Plasma membrane-associated receptors confer the first line of defense. Microbe associated molecular patterns or damage-associated molecular patterns are recognized by transmembrane receptors. Successful recognition of MAMP/DAMP by pattern recognition receptors leads to the activation of defense responses and termed as PAMP-triggered immunity. Receptor-like proteins and receptor-like kinases function as pattern recognition receptors and play a pivotal role in plant growth and development and also primes against abiotic stresses.
These receptors detect highly conserved molecules: small peptides and carbohydrates. PTI defense responses include of production of reactive oxygen species (ROS), changes in plant cell wall structure, and induction of antimicrobial compounds that lead to the activation of signaling pathways.
Unlike receptor-like proteins, the intracellular receptors are more specialized and belong to nucleotide-binding site leucine-rich repeats (NBS-LRRs) and called as R-genes. These NLR proteins target the effector molecules or avirulence (Avr) factors of pathogens.
To combat these proteins, pathogens have developed specific tools that release Avr molecules into the plant cell and suppress NLR protein responses. The fruitful recognition of Avr-factors triggers the hypersensitive response which caused the programmed cell death (PCD) and ceases the pathogen at the infection site.
Effector triggered immunity (ETI) induced the production of mobile immune signals: salicylic acid (SA), azelaic acid, and glycerol-3-phosphate (G3P). These molecules transport the immune signals from the infection site to uninfected sites and lead to the massive accumulation of SA and transcriptional reprogramming. Ultimately, transcriptional reprogramming induces a mechanism called systemic acquired resistance (SAR) which initiates the production of pathogenesis-related proteins (PR-proteins).
The programmed cell death successfully limits the biotrophic pathogens. The receptor-like kinases and receptor-like proteins are present in all three domains of life but in a larger amount in eukaryotes.
Receptor-like kinases structurally are consisting of three domains: one is extracellular ligand-binding that recognizes the invasion patterns, second is transmembrane domain and third is an intracellular cytoplasmic kinase for downstream signaling. The cell surface immune receptors are classified as a receptor-like kinase (RLK) and receptor-like proteins (RLP) on the basis of kinase activity in their cytoplasmic tail.
Signal transduction during cell surface receptor-mediated immunity can be achieved through phosphorylation cascades of MAP Kinases and calcium-dependent protein kinase.
Regulation of Cell Surface Immune Receptors
Cell surface immune receptors are regulated by the following mechanisms:
- Transcriptional and Epigenetic
- Post-transcriptional
- Post-translational regulatory mechanisms
At the transcriptional level, the immune receptors are induced by ergosterol and squalene by symbiont, Trichoderma. In Solanaceous crop plants e.g.; mungbean the receptor-like kinase/receptor-like proteins and NLR genes are induced by wounding, treatment with hormones, and pathogen infection. Post-transcriptional regulation occurs by alternative splicing. And post-translational regulation includes differential protein modifications, protein degradation, protein stabilization, and protein trafficking. The three regulatory mechanisms precede the immune responses in a controlled and stable manner.
Intracellular immune receptors that bind with effector molecules are induced by PAMP-triggered immunity, hormone treatment, and by various stresses or injuries. Intracellular immune receptors are classified into various types on the basis of their conserved domains. “The nucleotide-binding domain (NB-ARC; nucleotide-binding adaptor shared by APAF-1, R proteins, and CED-4) and leucine-rich repeat (LRR) are located in the central and C-terminal regions of these immune receptors. These NB-LRR receptors or NLRs could be divided into TNL (TIR-NB-LRR; Toll/interleukin-1 receptor-nucleotide-binding-leucine-rich repeat) and CNL (CC-NB-LRR; coiled coil-nucleotide-binding-leucine-rich repeat) subgroups by the presence of additional N-terminal domains, TIR domain or CC domain, respectively.”
Recognition of effector molecules by these intracellular proteins induces the gene-for-gene resistance. NB-LRR proteins can recognize effector molecules directly by physical association or indirectly by helper proteins. In an indirect method, the effector modifies an accessory protein which maybe its target.
The activation of these two phenomena as plant defense leads to a rapid influx of calcium ions, a burst of reactive oxygen species, activation of mitogen-activated protein kinases, gene expression programming, and cell death by the hypersensitive response. Gene expression signature of both PTI and ETI are similar which suggests that both (PTI and ETI) are similar but vary in their magnitude.
