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Part of the book series: Nucleic Acids and Molecular Biology ((NUCLEIC,volume 21))

Potential pathogens deliver effector proteins into plant cells to suppress microbe-associated molecular pattern (MAMP)-triggered immunity in plants, resulting in host—pathogen coevolution. To counter pathogen suppression, plants evolved disease resistance (R) proteins to detect the presence of the pathogen effectors and trigger R-dependent defenses. Most isolated R genes encode proteins possessing a leucine-rich-repeat (LRR) domain, of which the majority also contain a nucleotidebinding site (NBS) domain. There is structural similarity and/or domain homology between plant R proteins and animal immunity proteins, suggesting a common origin or convergent evolution of the defense proteins. Two basic strategies have evolved for an R protein to recognize a pathogen effector (then called avirulence factor; Avr): direct physical interaction and indirect interaction via association with other host proteins targeted by the Avr factor. Direct R-Avr recognition leads to high genetic diversity at paired R and Avr loci due to diversifying selection, whereas indirect recognition leads to simple and stable polymorphism at the R and Avr loci due to balancing selection. Based on these two patterns of R-Avr coevolution, investigation of the sequence features at paired R and Avr may help infer the R-Avr interaction mechanisms, assess the role and strength of natural selection at the molecular level in host—pathogen interactions and predict the durability of R gene-triggered resistance.

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Xiao, S., Wang, W., Yang, X. (2008). Evolution of Resistance Genes in Plants. In: Heine, H. (eds) Innate Immunity of Plants, Animals, and Humans. Nucleic Acids and Molecular Biology, vol 21. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-540-73930-2_1

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