RPS5-mediated disease resistance in the plant Arabidopsis thaliana

To successfully resist pathogen infection, plants need to recognize the pathogen and then induce defense responses that protect it from disease. Previous research has demonstrated that pathogen recognition is mediated by several distinct families of functionally variable, but structurally related plant disease resistance {dollar}(R){dollar} genes. From the plant Arabidopsis, I have isolated the {dollar}R{dollar} gene {dollar}RPS5{dollar}, which is a member of the largest family of {dollar}R{dollar} gene-encoded proteins. This family is defined by the presence of a putative nucleotide binding domain and a variable number of leucine rich repeats (LRRs). The function of these LRRs has not been established, but they are speculated to bind pathogen-derived ligands. A mutation in RPS5 was identified that indicated the LRR region may interact with other plant proteins. The rps5-1 mutation caused a glutamate to lysine substitution in the third LRR, and partially compromised the function of several {dollar}R{dollar} genes that confer bacterial and downy mildew resistance. Since the third LRR was relatively well conserved among {dollar}R{dollar} gene encoded proteins, it is speculated that this region may interact with a signal transduction component shared by multiple {dollar}R{dollar} gene pathways. This component has not been identified, but three candidate genes were identified in a mutant screen that assayed for loss of RPS5 function. The PBS1 gene product appears to be closely associated with pathogen recognition conferred by RPS5, while PBS2 and PBS3 are potential signal transduction genes that are required for disease resistance specified by multiple bacterial and downy mildew resistance genes. PBS3 also seems to be necessary to restrict the spread of virulent pathogens. Further dissection of signal transduction pathways mediated by R genes should continue to increase our understanding of molecular mechanisms used by plants to resist pathogen infection.