Evolution of the Plant R Gene System

Plant innate immunity consists of preformed physical and chemical barriers (such as leaf hairs, rigid cell walls, pre-existing antimicrobial compounds) and induced defenses. Should an invading microbe successfully breach the preformed barriers, it may be recognized by the plant, resulting in the activation of cellular defense responses that stop or restrict further development of the invader (Nurnberger et al. 2004). Apart from virus-induced RNA silencing, an ancient, evolutionary conserved antiviral defense mechanism in both plants and animals (which is not discussed in this chapter), two evolutionarily interrelated mechanisms have evolved in plants for detection of the invading microbes. First, plants are able to recognize some conserved microbe-derived molecules which are collectively described as microbe-associated molecular pattern (MAMP) by cell-surface receptors and trigger immune response (Gomez-Gomez and Boller 2000; Zipfel et al. 2006). Evidence is accumulating that this so-called MAMP-triggered immunity (MTI) is evolutionarily ancient and may be a general feature of plant resistance against a broad-spectrum of potential pathogens (Nurnberger et al. 2004; He et al. 2006). This type of resistance occurs at or above the species level, and is often referred to as non-host resistance. It can be envisaged that microbes that successfully breached constitutive defensive barriers of plants but were restricted by MTI gradually evolved strategies to target and sabotage the MTI. Increasing evidence indicates that successful microbes suppressed MTI by sending effector proteins into the plant cell to interfere with the host defense system, resulting in the breakdown of non-host resistance and the establishment of a host-pathogen interaction. The "defeated" host then faced selection pressure imposed by the successful pathogen to evolve novel defense mechanism to survive. This led to the evolution of the second recognition mechanism for which plants evolved disease resistance (R) proteins to specifically detect the presence of the pathogen effectors [called avirulence factors (Avr) once recognized by R proteins] and subsequently trigger a much stronger defense response to counter the suppression of MTI by the pathogen (Chisholm et al. 2006). Thus, R gene-dependent, pathogen-effector-iriggered host immunity (ETI) most likely evolved on top of MTI to fortify the plant immune system. Recent publications strongly support this inference (Kim et al. 2005; He et al. 2006; Nomura et al. 2006). For example, He and colleagues recently found that HopMl, a conserved effector protein of Pseudomonas syringae, targets an immunity-associated protein, AtMIN7 in Arabidopsis thaliana. HopMl mediates the destruction of AtMIN7 via the host proteasome (Nomura et al. 2006). Sheen and colleagues found that AvrPto and AvrPtoB, two effector proteins of the bacterial pathogen P syringae suppress MTI at an early step upstream of MAPK signaling (He et al. 2006). Both AvrPto and AvrPtoB are recognized by the plant R protein Pto in tomato, thereby triggering Pto-dependent resistance (Kim et al. 2002).

Evolution of the ETI system in plants marks a higher level of plant-pathogen coevolution in which the major players are plant R and pathogen Avr genes. Unlike MTI, which is expressed in all plants of a given species, ETI is often expressed in some but not all genotypes within a plant species. This correlates to the phenomenon that there are often two likely outcomes from a given host-pathogen interaction: (a) compatible interaction in which the pathogen is able to suppress host defenses and colonize the plant; (b) incompatible interaction in which the pathogen is detected by the plant containing an R gene and the plant is resistant. Therefore, genetically defined R genes are polymorphic determinants of host resistance against specific pathogens.

MTI in plants resembles the innate immune system of animals in that structurally similar cell-surface receptors are deployed to recognize MAMPs such as flagellin and lipopolysaccharides and the induction of host defenses involves MAPK signaling cascades (Nurnberger et al. 2004). Thus, MTI seems to be a highly conserved defense mechanism evolved in both plants and animals. Interestingly, so far there is no clear evidence to indicate the existence of ETI in animals. Therefore, it appears that the evolution of an elaborative plant ETI system in which a large array of R proteins function as receptors to recognize pathogen-specific effectors constitutes an important distinction between the plant and animal innate immune systems (Ausubel 2005). This probably reflects the consequence of adaptive evolution: plants are sessile, lack a circulating system and live relatively longer than most invertebrate animals; thus evolution of a greater capacity in every single cell to respond and mount effective defenses against numerous microbial invaders seems to be a logical choice for plants.

In the following sections, we focus our review on the current understanding of evolution and maintenance of plant R genes within the context of concomitant evolution of pathogen Avr genes that interact with R genes. For detailed molecular mechanisms of R gene evolution, we strongly recommend several excellent earlier review articles (Michelmore and Meyers 1998; Bergelson et al. 2001; Holub 2001; Meyers et al. 2005).

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