Tremendous progress has been made in understanding the evolution and molecular mechanism of plant R gene-based resistance (Hammond-Kosack and Parker 2003; Chisholm et al. 2006; this chapter). Many important questions regarding R gene evolution, R-Avr recognition and defense signaling remain to be addressed. These include when and how the earliest plant NBS-LRR genes originated, whether NBS-LRR genes function in MAMP recognition or other cellular processes, how MTI and ETI are connected at the molecular level, what other components are in the R recognition complex and why TIR-NBS-LRRs are absent in monocots. Also not known is whether atypical R genes represent host targets and activate NBS-LRR-dependent defenses or involve different defense mechanisms through novel yet unidentified signaling pathways.
What can we learn from our current knowledge about the plant R gene system at the molecular level to improve disease control for agricultural crops? First, based on the R-Avr coevolution, R genes recognizing Avr genes via direct R-Avr interaction may be easily overcome by mutations in cognate Avr genes; thus monoculture with crops of such genotypes may be subject to high risk of epidemics caused by virulent pathogens carrying mutated versions of Avr genes. Given that genetic diversity at the R gene loci is the consequence of R-Avr coevolution in natural plant populations and is important for the generation of new R genes or alleles, it would be a better strategy to grow crop cultivars containing distinct R genes or R alleles in a mixed structure (polyculture) which resembles the natural plant populations, thereby preventing disease epidemics and reducing disease incidence (Dangl and Jones 2001). The potential of this strategy has been demonstrated in rice to control bacterial blight (Zhu et al. 2000).
Second, identification and deployment of durable R genes is a primary target of crop breeding programs. However, there is no easy way to assess and predict the durability of R genes. A high fitness penalty of Avr genes in the pathogen could be used for predicting the durability of the cognate R genes (Leach et al. 2001), as a high fitness penalty would set constraints for Avr genes to escape from R recognition. But it may not be accurate in situations where Avr genes directly recognized by R genes may evade recognition by mutations that do not necessarily affect its virulence function (see Section 6.1). Also it may be practically difficult to assess the fitness penalty of Avr genes. One of the most exciting inferences from R-Avr coevolution is that R-Avr indirect recognition leads to stable balanced polymorphisms at the R and Avr loci (Table 2), which implies that R genes of this category are likely to be durable. Even though this rule needs to be vigorously tested with more R and Avr pairs, it gives a promising molecular tool to identify and predict durable R genes that guard critical virulence targets based on the feature of the sequence polymorphism in the natural plant populations (Dangl and McDowell 2006). Comparative genomic analyses have identified two types of NBS-LRR genes based on the rate of sequence diversification: fast evolving and slow evolving (Kuang et al. 2004, 2005). A key question is: would the existence of these two types of NBS-LRR genes reflect the two paths of R gene evolution largely determined by the two different R-Avr recognition mechanisms in general? If true, prediction of R recognition mechanism and resistance durability by coupling data from genetic mapping and sequence polymorphism could be applied at the whole genome scale.
Third, the natural evolution of R genes that recognize new or mutated Avr genes is after all a slow process. If such R gene resources are unavailable from natural plant populations, a viable strategy is to generate R genes artificially in laboratories by in vitro mutagenesis or sequence shuffling with relevant existing genes/alleles and to screen for DNA clones that can induce target Avr-dependent HR through transient coexpression with cognate Avr genes in a suitable host. Such synthetic genes may function as new R genes in the native host to recognize the pathogens carrying newly mutated versions of Avr genes and can be introduced to desirable plant cultivars through genetic transformation.
Acknowledgements We would like to thank Donald Nuss and Dacheng Tian for critical review and valuable comments on the manuscript. Work in S.X.'s laboratory is supported by the National Research Initiative of the USDA Cooperative State Research, Education and Extension Service, Grants 2005-35319-15656 and 2006-35301-16883.
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