Introduction
Like all other living organisms, plants are also constantly engaged in a struggle for protecting themselves from pathogens, by adapting various immune strategies. The capacity of plants to defend themselves against pathogens, differs largely from mammals primarily due to their fundamental biological differences. Plants are sessile, requiring pathogen mobility where as mammals are mobile and hence are able to spread infections by contact. In addition, mammals have adaptive immunity enabling them to target the pathogens specifically. Intriguingly, no adaptive immune system which is equivalent to the highly complicated vertebrate immune system has been found in plants. Yet, the fact that a plethora of plant species exist till date, evokes an idea that plants in fact, have highly effective system of defense against pathogen invasion and disease. Despite these and other differences, plant disease resistance and mammalian innate immunity share several remarkable similarities. Plants possess physical and chemical barriers such as a thick cell wall made of lignin, a cuticle, secrete chemical compounds such as saponins which offer non-specific protection against a pathogen. It is integral to gain insights into various plant-pathogen interactions from the perspective of both the organisms, to understand how they coevolve for dominance over each other.
Plants are exposed to and invaded by diverse pathogens, including bacteria, fungi, viruses and nematodes. These pathogens cause various diseases, some of which show visible symptoms such as leaf spots, powdered mildew, leaf rust etc. While some diseases result in death of the plant, most of the diseases perturb its growth and development. One of the phenomena of plant disease resistance, is rapid cell death at the site of infection called, the Hypersensitive Response (HR) which is often compared with animal programmed cell death. Indisputably, this is the most effective process at limiting pathogens that require living host cells. Some resistance responses such as activation of defense gene expression eventually leading to the production of antimicrobial proteins or low molecular weight antibiotics is comparable to that of the innate immune system in insects and vertebrates.
Pathogen-Associated Molecular Patterns (PAMPs), as the name suggests are generic signals of the presence of pathogen and act as elicitors for plant’s basal defense. Some examples include fungal chitin, bacterial lipopolysaccharides, flagellins [1,2] and more recently, these have been coined the term Microbe-Associated Molecular Patterns (MAMPs), as some of the non-pathogenic microorganisms also have PAMPs [3]. Resistance (R) genes is another mechanism by which plants detect pathogen infection and mount an effective immune response. The products of R genes interact with products of Antivirulence (Avr) genes that are present in the pathogen, either directly or indirectly. The products of Avr genes cause avirulence in the presence of R gene products and hence the name and recognition of Avr proteins by plants is called effector-triggered immunity in contrast to (PAMP)-triggered immunity(Chisholm et al., 2006; Jones and Dangl, 2006). In the absence of a cognate R gene, avr gene products contribute to virulence, although they are not important for pathogen viability. Disease resistance is observed if the product of any particular R gene has recognition specificity for a product produced by a particular pathogen Avr gene.
The Guard to Decoy Model
The classic concept of gene for gene relationship, offering plant disease resistance requires the presence of two complementary genes: Avr genes in pathogen and a matching R gene in the host. The direct interaction between Avr gene product and a corresponding R gene product occurs less frequently compared to that of the indirect interaction and can be called as a receptor-ligand model where R protein acts as a receptor for Avr protein (Keen 1990). In fact, direct binding for many R-Avr interactions was found consistent with the receptor-ligand model (Jia et al., 2000; Deslandes et al., 2003; Dodds et al., 2006; Ueda et al., 2006). For a number of R-Avr interactions, failure to detect direct interaction led to the Guard hypothesis which proposes that the target of Avr protein, also called as a guardee is protected by the R protein. When the guardee is modified by the effector target (Avr protein), it activates the R protein, which triggers disease resistance in the host (Figure 1A, Dangl and Jones, 2001). The Guard Model was originally proposed to explain the mechanism of Pseudomonas syringae, AvrPto interaction with the tomato proteins Pto and Prf (Van der Biezen and Jones, 1998) and was later generalized to other effector proteins. Intriguingly, small R gene repertoire can perceive multiple effectors of a broad diversity of pathogens that attack plants (figure 1B).
The guardees, illustrated in the guard model undergo a series of duplication events and subsequently, evolve independently to become decoys of the effector targets. Studies have shown that these decoys, mimic the guardees and are free from non-immune cellular functions that these proteins originally have (Vandern Hoorn, 2008). Also, they evolve to become better triggers for corresponding guard R protein, thus acting as an effective bait for pathogen effectors (Ashkenazi A. 2002).
References:
• Keen, N.T. (1990). Gene-for-gene complementarity in plant-pathogen interactions. Annu. Rev. Genet. 24 447–473.
• Jia, Y., McAdams, S.A., Bryan, G.T., Hershey, H.P., and Valent, B. (2000). Direct interaction of resistance gene and avirulence gene products confers rice blast resistance. EMBO J. 19 4004–4014.\
• Deslandes, L., Olivier, J., Peeters, N., Feng, D.X., Khounlotham, M., Boucher, C., Somssich, I., Genin, S., and Marco, Y. (2003). Physical interaction between RRS1-R, a protein conferring resistance to bacterial wilt, and PopP2, a type III effector targeted to the plant nucleus. Proc. Natl. Acad. Sci. USA 100 8024–8029.
• Dodds, P.N., Lawrence, G.J., Catanzariti, A.M., Teh, T., Wang, C.I., Ayliffe, M.A., Kobe, B., and Ellis, J.G. (2006). Direct protein interaction underlies gene-for-gene specificity and coevolution of the flax resistance genes and flax rust avirulence genes. Proc. Natl. Acad. Sci. USA 103 8888–8893.
• Ueda, H., Yamaguchi, Y., and Sano, H. (2006). Direct interaction between the tobacco mosaic virus helicase domain and the ATP-bound resistance protein, N factor, during the hypersensitive response in tobacco plants. Plant Mol. Biol. 61 31–45.
• Chisholm, S.T., Coaker, G., Day, B., and Staskawicz, B.J. (2006). Host-microbe interactions: Shaping the evolution of the plant immune response. Cell 124 803–814.
• Jones, J.D.G., and Dangl, J.L. (2006). The plant immune system. Nature 444 323–329.
• Dangl, J.L., and Jones, J.D.G. (2001). Plant pathogens and integrated defense responses to infection. Nature 411 826–833.
• Van der Biezen, E.A., and Jones, J.D.G. (1998). Plant disease-resistance proteins and the gene-for-gene concept. Trends Plant Sci. 23 454–456.
• van der Hoorn, R. & Kamoun, S. 2008 From guard to decoy: A new model for perception of plant pathogen effectors. The Plant Cell 20, 2009–2017.
• Ashkenazi, A. 2002 Targeting death and decoy receptors of the tumour-necrosis factor superfamily. Nature Reviews Cancer 2(6), 420–430.
•