Over the course of history plant disease has been responsible for devastating famines, today crop yields continue to be reduced to due infection with plant pathogens. Plants lack a circulating immune system; instead they have evolved other methods of fending off disease. The first lines of defense are the chemical and physical barriers on the exterior of the plant such as a waxy coat. Plants further defend themselves against pathogens via specific gene-for-gene interactions. If a pathogen contains an avirulence (avr) gene that complements a resistance (R) gene in the plant then the plant can respond to the threat. However if one or both of these genes are missing, the response cannot occur. An activated R gene triggers a suite of defense responses, including the hypersensitive response (HR). The HR is a signal mediated programmed cell death occurring around the site of infection. Our study is devoted to RPM1, an R gene of Arabidopsis thaliana. We have shown that the RPM1 gene product, Rpm1, degrades coincident with the HR. In order to gain more insight into the role of RPM1 in the plant disease resistance pathway we have observed the degradation patterns of Rpm1 in various mutant backgrounds when inoculated with the bacteria Pseudomonas syringae carrying plasmids encoding avrRmp1, avrRpt2, or avrRps4. Some mutants that disrupt signaling induced by R-genes also disrupt degradation of Rpm1. Other mutants that disrupt the HR do not block degradation or Rpm1. Therefore Rpm1 degradation is not an inadvertent consequence of the HR. We postulate that activation of R-genes triggers the Rpm1 protein to be ubiquinated. Once tagged with ubiquitin it becomes a target for proteosome digestion. Indeed, inhibition of the proteosome blocks degradation of Rmp1 also and enhances cell death in response to Rpm1 activation. In conclusion, degradation of Rpm1 is a regulated process which desensitizes the plant cells, and thereby limits the extent of HR-induces death around an infection site.