Pathogen-Associated Molecular Pattern-Triggered Immunity: Veni, Vidi…?

For many years, plant pathology was divided into two schools of thought. It was clear that purified molecules or crude extracts from microbes or plants (referred to as general elicitors) could induce activation of general defense responses (Boller, 1995). Geneticists instead were studying plant resistance triggered by the recognition of a given pathogen Avirulence gene product by the corresponding plant Resistance (R) gene product (Dangl and Jones, 2001). This resistance followed the gene-for-gene hypothesis, was often associated with a hypersensitive response, and was widely used in breeding programs. It was however confusing why a pathogen would produce Avirulence products that would cause its recognition and subsequent host resistance. By the end of 1990s, most classical general elicitors were oligosaccharides or glycoproteins (Boller, 1995). The identification of protein elicitors and their corresponding epitopes allowed a more thorough analysis of their conservation among the increasing amount of genomic information. For example, bacterial flagellin (the main building block of the flagellum) activated defense responses in tomato (Solanum lycopersicum) and Arabidopsis (Arabidopsis thaliana) and a peptide of 22 amino acid (flg22) conserved in many bacterial species was sufficient to trigger the full set of defense responses (Boller and Felix, 2009). Together with the demonstration that nonprotein pathogen-associated molecular patterns (PAMPs), e.g. lipopolysaccharides, classical activators of innate immune responses in animals, also induce defense responses in plants, it became evident that general elicitors resembled PAMPs (Nürnberger and Brunner, 2002). These were defined as conserved molecules present in whole classes of microbes (nonself) with an essential function for these microbes (Medzhitov and Janeway, 1997).