References

100 T. Nürnberger, B. Kemmerling
pattern recognition modules that universally mediate perception of ligands
of all chemical kinds. As plants possess 235 LRR-RLKs (Shiu and Bleecker
2001), a significant number of those proteins are expected to serve PAMP
perception in plants.
Loss of flagellin perception in Arabidopsis resulted in enhanced disease
susceptibility (reduced basal resistance) against the virulent bacterial
strain, Pseudomonas syringae pv. tomato DC3000 (Zipfel et al. 2004). This
is important as it indicates that PAMP perception actively contributes to
basal (or plant species-specific) immunity and that single PAMP recognition
events already affect the severity of microbial infections on susceptible
host plants. Eventually, this efficiency may explain why suppression of
PAMP-mediated immunity evolved as a major strategy of microorganisms
to establish susceptibility on host plants.
7.4
Pathogen Recognition in Host Cultivar-Specific Resistance
AcurrentmodelsuggeststhatPAMP-inducedplantspecies(nonhost)resistance
was incapacitated by microbial pathogens through the acquisition of
virulence factors which enabled them to colonize susceptible hosts through
suppression of innate immune defenses (Espinosa and Alfano 2004). In
turn, evolution of new pathogen race-specific virulence factors have driven
the coevolution of plant cultivar-specific resistance genes and thus development
of phylogenetically more recent pathogen race/plant cultivar-specific
disease resistance (Dangl and Jones 2001; Van der Hoorn et al. 2002). The
genetic basis for plant cultivar-specific disease resistance is determined
by gene pairs called pathogen-derived avirulence (Avr)genesandplantderived
resistance (R)genes.Avr gene-encoded proteins are likely (sometimes
dispensable) effectors that contribute to host infection, although their
biochemicalmodeofactioninmanycasesremainselusive.Inthosecases
when Avr factors are recognized by resistant host plant cultivars through
interaction with their complementary R gene-encoded protein counterparts,
they act as specific elicitors of plant defense rather than virulence or
pathogenicity factors and betray the potential phytopathogen to the host
surveillance system.
A simple biochemical interpretation of this gene-for-gene hypothesis
would be a receptor/ligand-like interaction between plant R gene products
and the corresponding pathogen-derived Avr gene products. Direct interaction
between AVR proteins and R proteins was indeed shown (Cohn et
al. 2001; Jia et al. 2000), but nevertheless represents an exception rather
than the rule in R-gene-dependent plant immunity. Molecular analyses of
numerousplant–microbeinteractionsrevealedthatthesituationislikely