Plant signaling pathways activating defence response and interfering mechanisms by pathogen effectors, protein decoys and bodyguards

摘要

Plants activate an immune response in defense against microbial pathogens. The first layer of immunity consists in the recognition of microbial fingerprints, called Pathogen Associated Molecular Pattern (PAMP), by a set of Pattern Recognition Receptors (PRR). In addition, the degradation products from fungi, bacteria and plant cells are recognised as Damage Associated Molecular Pattern (DAMP). The first layer of plant defence is based on Pattern Recognition Receptors (PRR) on the membrane. These receptors, either receptor kinases or receptor-like proteins (RLPs), associating with cytoplasmic kinases, recognize the presence of PAMPs, thus activating a local response named PAMP-triggered immunity (PTI), that is not strong but effective towards many pathogen species. Here we discuss and focus on Elongation Factor Tu Receptors (EFR) and flagellin sensing (FLS) receptors. In leucine-rich repeat (LRR) receptor proteins, the hydrophobic LLR domains are exposed on external membranes, providing the protein-protein interaction modules. Plants evolved this protein-protein interaction domain several times during the development of mechanisms to defend themselves from viruses, virulence factors, enzymes and effectors of bacterial and fungal pathogens. Pathogens in addition evolved proteins and enzymes that are injected in the plant cell to counterfight plant immune signaling pathways. These effectors are recognised by plant receptors sensing their presence of their cognate avirulence genes. These receptors originated from recombination during evolution and only occur in some specific tomato genotypes, instead of the widely occurring PPRs. Effector Triggered Immunity (ETI) allows a plant response to effector proteins that is more strong, but is race specific. It leads to local necrosis and apoptosis, and to the establishment of the hypersensitive response (HR). For biotrophic or hemibiotrophic pathogens, necrosis is an effective way to limit their spread, while for necrotrophic pathogens this is not efficient and sufficient way to limit their spread, since depends on the timing of infection and on the plant development phase. Pathogenic fungi strategy relies on the formation of specialised structures, or haustoria, that facilitate the nutrient uptake form plant cells. In this review, we summarize the most recent knowledge on plant pathogens and the mechanisms they evolved to circumvent plant defences among which pathogen effectors, protein decoys inactivating plant defence signals. Effectors are recognised through their binding to plant proteins by means of plant receptors, that activate the Effector Triggered Immunity (ETI). In particular, we focus on the Solanaceae, discussing general mechanisms and specific pathways that confer resistance to various pathogens. There is an arm race between plants and fungal and bacterial pathogens that has led to new protein variants and protein decoys (pseudokinases, inhibitors and sponges blocking glucanases, and Transcription Activator Like Effectors). Advances in understanding the function of pathogen effectors will provide new ways to improve plant immunity and mechanisms of defence against their pests. Finally, we present possible combinations of interventions, from gene engineering to chemical priming, acting on signaling pathways regulated by jasmonate and salicylate hormones, to increase plant resistance and activate plant defences without affecting crop yields.