Like animals, plants are able to recognize highly conserved features of microbes known as microbe-associated molecular patterns (MAMPs). MAMPs are typically necessary for and integral to microbial lifestyles and are therefore not easily lost or mutated, making them ideal targets for detection by plant immune receptors. For example, both plants and animals can detect the presence of Gram-negative bacteria through the perception of lipopolysaccharides (LPSs) found in their outer membrane (Dow et al. 2000) . Plants respond to other MAMPs including peptides or motifs characteristic to bacterial proteins such as flagellin, elongation factor Tu (EF-Tu), and cold shock proteins, as well as to sugars found in bacterial and fungal cell walls (peptidoglycan and chitin, respectively; reviewed in Nürnberger et al. 2004). Thus, plants have evolved the ability to differentiate between self and non-self as part of an early warning system against potential pathogen infection.
MAMPs are recognized in mammals by transmembrane Toll-like receptors (TLRs) and cytosolic Nod proteins (Akira et al . 2006). collectively referred to as pattern or pathogen recognition receptors (PRRs). In plants, transmembrane receptor-like kinases (RLKs) play an integral role in MAMP perception and signal relay. Two PRRs that have been well characterized in plants include FLS2 (FLAGELLIN-SENSITIVE2; Gómez-Gómez and Boller 2000), and EFR (EF-Tu RECEPTOR; Zipfel et al. 2006), which recognize bacterial flagellin and EF-Tu, respectively. FLS2 and EFR have an extracellular leucine-rich repeat (LRR) domain and a cytosolic serine/threonine kinase domain, and likely represent members of a larger group of RLKs involved in MAMP perception (Zipfel 2008). Plants respond to MAMPs rapidly with pronounced changes in gene expression, cell wall alterations, accumulation of antimicrobial proteins and compounds, and changes in apoplastic pH levels that hinder the growth of microbial populations to some extent but are only slightly effective at preventing the growth of virulent pathogens (Gómez-Gómez and Boller 2000).
Bacterial pathogenesis is largely reliant on the ability to move into and within the plant apoplast, and this motility is provided by flagella. FLS2 proteins in Arabidopsis, tomato, and tobacco recognize and respond to bacterial flagellin, indicating that this recognition module is conserved across plant species (Zipfel 2008). FLS2 in Arabidopsis binds a small but highly conserved 22-amino acid epitope, flg22, from the N-terminus of the flagellin protein (Chinchilla et al.2006). Arabidopsis plants treated with flg22 one day prior to infection with virulent bacteria exhibit a reduction in bacterial growth compared to plants that are not pre-treated; conversely, ñs2 mutants are unable to perceive and respond to the flg22 elicitor, which is reflected in the higher susceptibility of these plants to bacterial infection (Zipfel et al. 2004). The same phenomenon has been observed using the EF-Tu elf18 epitope as an elicitor (Zipfel et al. 2006), demonstrating that the detection of single MAMPs can prime cells against further attack.
PRR activation and downstream signaling are tightly controlled. FLS2 is negatively regulated by the kinase-associated protein phosphatase KAPP (Gómez-Gómez et al. 2001) at the plasma membrane, and is internalized following flg22 binding by vesicle-mediated endocytosis as part of a negative feedback regulation scheme (Robatzek et al. 2006) . Both FLS2 and EFR are positively regulated by another RLK, BAK1 (brassinosteroid-associated kinase 1; Chinchilla et al . 2007; Hesse et al . 2007) . Interestingly, both tobacco and Arabidopsis mutants with compromised FLS2 activity become susceptible to nonadapted pathogens (Zipfel 2008), suggesting that PRRs are integral to both host and nonhost resistance. Flagellin from the legume-associated nitrogen-fixing symbiont Rhizobium is not recognized in Arabidopsis by FLS2; nor is flagellin from the plant pathogen Agrobacterium (Felix et al.1999) , indicating that microbes are under evolutionary pressure to alter MAMPs to avoid recognition by the host PRR surveillance system.
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