It was proposed by Harold Henry Flor[1][2][3][4] who was working with rust (Melampsora lini) of flax (Linum usitatissimum).
Flor showed that the inheritance of both resistance in the host and parasite ability to cause disease is controlled by pairs of matching genes.
[8] The protein products of the NBS-LRR R genes contain a nucleotide binding site (NBS) and a leucine rich repeat (LRR).
The protein products of the PRRs contain extracellular, juxtamembrane, transmembrane and intracellular non-RD kinase domains.
LRRs are multiple, serial repeats of a motif of roughly 24 amino acids in length, with leucines or other hydrophobic residues at regular intervals.
[13] LRRs are involved in protein-protein interactions, and the greatest variation amongst resistance genes occurs in the LRR domain.
Because there would be no evolutionary advantage to a pathogen keeping a protein that only serves to have it recognised by the plant, it is believed that the products of Avr genes play an important role in virulence in genetically susceptible hosts.
[19] AvrPto is an ancient effector that is conserved in many P. syringae strains, whereas Pto R gene is only found in a few wild tomato species.
This lack of evidence for a direct interaction led to the formation of the guard hypothesis for the NBS-LRR class of R genes.
Several experiments support this hypothesis, e.g. the Rpm1 gene in Arabidopsis thaliana is able to respond to two completely unrelated avirulence factors from Pseudomonas syringae.
Another high profile study that supports the guard hypothesis shows that the RPS5 pair uses PBS1, a protein kinase as a guardee against AvrPphB.