Resurrecting potato R3a: expanded response to Phytophthora effectors

MARINA FRANCESCHETTI; SEGRETIN, MARÍA EUGENIA; PAIS, MARINA; CHAPARRO GARCÍA, ANGELA; JORUNN I.B. BOS; MARK J BANFIELD; KAMOUN, SOPHIEN

Rodas

Congreso; XVI International Congress on Molecular Plant-Microbe Interactions; 2014

IS-MPMI

Nucleotide-binding leucine-rich repeat-containing proteins (NB-LRRs) mediate effector trigger immunity in plants. Pathogens are engaged in a co-evolutionary arms race with their host, continuously evolving new effector variants to evade NB-LRR immunity or suppress host defences. Resistance genes against Phytophthora infestans from various wild potatoes have been widely used in plant breeding programs. However, these genes have been rapidly defeated by new virulent races of P. infestans and are of limited value in modern agriculture. The potato NB-LRR immune receptor R3a can only be activated by the K80/I103 isoform of the P. infestans effector Avr3a (Avr3aKI), while the current predominant allele E80/M103 (Avr3aEM) is not detected. As a first step to resurrect R3a, and to study how it responds to AVR3a, we undertook a gain-of-function random mutagenesis screen of this resistance protein. We identified 8 single mutations that extended the R3a response to the AVR3aEM isoform, and to other artificial AVR3a variants, while retaining the ability to detect AVR3aKI. These mutations occur across the whole R3a protein, from the N-terminus to different regions of the LRR domain, possibly interfering with different aspects of the effector response mechanisms. Remarkably, the N336Y mutation, near the nucleotide-binding pocket, conferred response to the Phytophthora capsici effector PcAVR3a4. Our work confirms that is possible to produce synthetic alleles of NB-LRR proteins with expanded specificity. The ability to modulate and extend a disease resistance gene response to a wider range of effectors offers the opportunity to develop broad-spectrum solutions to plant pathogens.