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Higher plants are hosts to all major classes of pathogens, fungi, oomycetes, bacteria, viruses, insects and worms (Figure 1). Microbial plant pathogens exhibit a range of life styles from biotrophs, whose proliferation depends on living host cells, to necrotrophs triggering tissue maceration. Biotrophic pathogens include bacteria, filamentous fungi and oomycetes causing diseases such as bacterial speck, powdery and downy mildew, respectively. Many plant cultivars used in agriculture are susceptible to such pathogens. For example, tomato is infected by Pseudomonas syringae pv tomato, barley by the fungus Blumeria graminis, soybean by the oomycete Phytophthora sojae and potato by Phytophthora infestans. The latter was responsible for the famous potato famine in Ireland in 1845. Still today, these pathogens trigger serious losses in agriculture and costly treatment with chemicals is therefore necessary.
To increase our knowledge of plant resistance responses and pathogen subversion, intensive research is required. 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 2). 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.
These defence responses are associated with substantial rearrangements inside host cells (Figure 1). 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.
Our research group actually situated both at the Max-Planck-Institut für Züchtungsforschung in Cologne (www.mpiz-koeln.mpg.de) and at The Sainsbury Laboratory (www.tsl.ac.uk/) in Norwich, applies biochemical, genetic and cell biology approaches to better understand the dynamic signalling and cellular changes in plant-microbe interactions.
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Figure 1. Schematic overview of a plant cell and its membrane-bound compartments. A) Plants are hosts to all major pathogens like viruses, bacteria, oomycetes and fungi. ER = endoplasmic reticulum, outer grey line = cell wall. B) Filamentous pathogens germinate on the cell surface, penetrate through the cell wall, and trigger intracellular rearrangements – accumulation of cytoplasm, ER, Golgi, mitochondria, nuclear migration, and focal secretion of exosomes and peroxisomes beneath the penetration site - to exploit living plant cells for proliferation. Localization of chloroplasts, vacuoles and endosomes remain elusive. C) Successful pathogens establish haustoria inside the plant cell, which are encased by the extrahaustorial membrane. Most intracellular arrangements are unknown. Arrows indicate trafficking pathways; dashed arrow = focal accumulation (adapted from Frei dit Frey and Robatzek, 2009).
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Figure 2. Perception of microbes (as fungi and bacteria) 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 gene as bacterial 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).
