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FLS2-GFP
Plants are hosts to all major classes of pathogens (fungi, oomycetes, bacteria), which exhibit a range of life styles from biotrophs depending on living host cells, to necrotrophs triggering tissue maceration. Many plant cultivars used in agriculture are susceptible to biotrophic pathogens, and costly treatment with chemicals is necessary to prevent serious losses in yield.
Although the field of plant pathogen interactions has seen major advances resulting in a paradigm shift during recent years, many questions remain to be answered. It is now accepted that plants sense microbes initially according to their pathogen-associated molecular patterns (PAMPs) through cognate pattern recognition receptors (Figure 1). PAMP perception stimulates a plethora of defence responses accumulating in plant basal resistance, which is referred to as PAMP-triggered immunity (PTI). Adapted pathogens can successfully suppress PAMP-triggered immunity with the help of secreted effector molecules leading to host disease. Certain plant cultivars, however, recognize the action of effectors from specific pathogen strains and thereby mount a potentiated defence response, known as effector-triggered immunity (ETI), which results in rapid local cell death to prevent further pathogen spread.
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Figure 1. Perception of microbes induces an active plant defence response called innate immunity (PTI). It involves physiological, molecular and genetic responses as well as ion fluxes, ROS production, stomatal closure, expression of defence genes. Pathogen effectors modify defence mechanisms and PTI signalling at any given level. (A) A plant leaf is schematically shown as top view (top) from cuticle and epidermis to cross-section through the apoplast and mesophyll cells (bottom). (B) A cross-section through one enlarged cell (adapted from Göhre and Robatzek, 2008).
These defence responses are associated with substantial rearrangements inside host cells (Figure 2). Subcellular changes often correlate with the formation of pathogen structures during the process of infection, as for the development of haustorial projections by filamentous pathogens. Furthermore, secretory and endocytic vesicle trafficking pathways in plants are rapidly changed in response to microbial infection. Ligand-induced endocytosis of the plasma membrane-resident pattern recognition receptor for bacterial flagellin, FLS2, was discovered, and appeared to be linked with PAMP signalling (Robatzek et al, 2006). This suggests an important role for endocytic trafficking in plant immunity.
Figure 2. Cell membrane compartmentalization is dynamic and instrumental for eukaryotic life. Pathogens proliferate on the cell surface, and attempted penetration triggers subcellular rearrangements – accumulation of cytoplasm, ER, Golgi, mitochondria, nuclear migration, and focal secretion of exosomes and peroxisomes beneath the penetration site. Successful pathogens deliver effector molecules into plant cells to reprogram host cellular life and promote disease. Filamentous pathogens project haustoria - feeding structures - inside the plant cell, but they remain which surrounded by the host’s membrane. Arrows indicate trafficking pathways; dashed arrow = focal accumulation; arrows with closed heads = effector delivery (adapted from Frei dit Frey and Robatzek, 2009).
Our research group situated at The Sainsbury Laboratory (www.tsl.ac.uk/) in Norwich, applies cell biology (Figure 3), genetic, and biochemical approaches to better understand the molecular mechanism of cellular changes in plant-microbe interactions.
Figure 3. High throughput imaging and computational cell detection. Puzzle-shaped Arabidopsis leaf epidermal cells.
