Evolution of Resistance Genes in Plants

Shunyuan Xiao(*ü), Wenming Wang, and Xiaohua Yang

1 Evolution of the Plant R Gene System 2

2 Conservation and Diversity of Plant R Genes 3

3 NBS, LRR and TIR - Domains of Defense 6

4 Proliferation and Diversification of NBS-LRR Genes in Plants 9

5 Mechanisms of R-Avr Recognition 10

5.1 Direct R-Avr Interaction - the "Gene-For-Gene" Hypothesis 10

5.2 Indirect R-Avr Interaction - the "Guard" Hypothesis 11

6 Patterns of R-Avr Coevolution 13

6.1 Diversifying Selection Results from Direct R-Avr Recognition? 14

6.2 Balancing Selection Results from Indirect Recognition? 15

6.3 A General Model for Evolution of the Plant R Gene System 17

7 New Perspectives 19

References 20

Abstract 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 nucleotide-binding 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 coevolu-tion, investigation of the sequence features at paired R and Avr may help infer the

Center for Biosystems Research, University of Maryland Biotechnology Institute, 9600 Gudelsky Drive, Rockville, MD 20850, USA, [email protected]

H. Heine (ed.), Innate Immunity of Plants, Animals, and Humans. Nucleic Acids and Molecular Biology 21. © Springer-Verlag Berlin Heidelberg 2008

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.

Abbreviations R, resistance gene; Avr, avirulence gene; HR, hypersensitive response; MAMP, microbe associated molecular patterns; MTI, MAMP-triggered immunity; ETI, Effector-triggered immunity; TIR, toll and interleukin receptor; NBS, nucleotide binding site; LRR, leucine rich repeat; RLP, receptor-like protein; RLK, receptor-like kinase

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