Host-microbe interactions: shaping the evolution of the plant immune response.
By S. Chisholm, G. Coaker, B. Day, B. Staskawicz. Cell, 2006
2,930 citations recorded by the source corpus.
The evolution of the plant immune response has culminated in a highly effective defense system that is able to resist potential attack by microbial pathogens. The primary immune response is referred to as PAMP-triggered immunity (PTI) and has evolved to recognize common features of microbial pathogens. In the coevolution of host-microbe interactions, pathogens acquired the ability to deliver effector proteins to the plant cell to suppress PTI, allowing pathogen growth and disease. In response to the delivery of pathogen effector proteins, plants acquired surveillance proteins (R proteins) to either directly or indirectly monitor the presence of the pathogen effector proteins. In this review, taking an evolutionary perspective, we highlight important discoveries over the last decade about the plant immune response.
Subfields: Plant Science
View Paper: https://www.semanticscholar.org/paper/461c04e9850f17ced513624c87cc4dc6a1eed740
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Citations in the corpus
- Salicylic Acid, a multifaceted hormone to combat disease. (2009, background): “Often, plants recognize an invading pathogen and mount an effective defense response by means of a direct or indirect interaction between the product of a host resistance (R) gene and its cognate pathogen-encoded effector protein; this is termed effector-triggered immunity (ETI, formerly termed R ge”
- Role of plant hormones in plant defence responses (2009, background): “As a counter defence strategy, plants recognise a given effector either directly or indirectly and activate effector-triggered immunity (ETI) resulting in disease resistance (Chisholm et al. 2006; Jones and Dangl 2006).”
- Firefly Luciferase Complementation Imaging Assay for Protein-Protein Interactions in Plants1[C][W][OA] (2007, background): “Bacterial pathogens inject effector proteins into the host cells to regulate host susceptibility/resistance to the bacterium (Chisholm et al., 2006; Nomura et al., 2006).”
- Rhizobacteria-induced systemic resistance (2009, background): “Perception ofMAMPs by pattern recognition receptors (PRRs) at the cell surface activates a battery of host defence responses leading to a basal level of resistance (Chisholm et al., 2006).”
- Signaling in Plant-Microbe Interactions (2013, background): “…protein Prf trigger resistance against P. syringae expressing effectors AvrPto and AvrPtoB whereas P. syringae strains having effectors AvrB or AvrRpm1, AvrRpt2 and AvrPphB trigger resistance in Arabidopsis plants carrying NB-LRR proteins RPM1, RPS2 and RPS5, respectively (Chisholm et al. 2006).”
- Salicylic Acid Biosynthesis and Metabolism (2011, background): “…on 04 Mar 2020 Terms of Use: https://bioone.org/terms-of-use can be envisioned as a ‘zig-zag’, in which the interplay between plant and pathogen leads to continued escalation of defenses and counter-defenses, respectively (Chisholm et al, 2006; Jones and Dangl, 2006; Nishimura and Dangl, 2010).”
- The Apoplastic Oxidative Burst Peroxidase in Arabidopsis Is a Major Component of Pattern-Triggered Immunity[W][OA] (2012, background): “The plant defense response has nowbeen dissected into several tiers of preexisting and/or activated defenses, many of which seem to involve the production of reactive oxygen species (ROS) (Chisholm et al., 2006; Jones and Dangl, 2006; He et al., 2007).”