49EVOLUTIONARY BIOINFORMATICS 2015:11 Background

Plants have evolved biotic stress sensory mechanisms that activate systemic and localized diseases-resistance responses.1 A disease-resistance response occurs when an elicitor, either a microbe-associated molecular pattern (MAMP) or a damage-associated molecular pattern (DAMP),2 activates the basal immune system in plants. Mechanism of action between disease-resistance genes (R-genes) and pathogen avirulence (Avr) genes was first described as the “Gene-for-Gene Model ” by Harold Flor in 1971. This model describes resistance as a function of an individual R-gene protein for a single pathogenic elicitor. Most of the R-gene proteins con-tain nucleotide binding-site (NBS) and leucine-rich region (LRR) domains, which are triggered by elicitors produced by pathogens, and then send a systemic signal to activate plant defense responses.3 Alternatively, the “Guard Model”4 describes NBS-LRR proteins serving as guards of certain proteins that are targets of pathogen elicitors. The “Zig-zag Model”4 describes the coevolution of pathogens and their prospective hosts: rapid adoption of one or more Avr proteins allows the pathogen to elude the host’s basal immune sys-tem until the plant produces appropriate NBS-LRR proteins for enhanced detection of the Avr elicitors.1 Rapid pathogen adaptation to the host defense system increases evolutionary pressure on the host at molecular level through gene duplica-tion, unequal crossing over, ectopic recombination, gene con-version, and diversifying selection.5–7 Plant disease resistance genes have recently been clas-sified into eight major families: 1) Nucleotide binding site (NBS)-leucine rich region(LRR)-Toll/interleukin-1-receptor