Summary: The results of this dissertation show that many RPP5 locus R genes, including SNC1, are coordinately regulated both positively and negatively, and that the locus-wide regulation involves a positive feedback mechanism as well as RNA silencing of paralogous R genes in the locus. Moreover, the results reveal that the bal allele was generated by a tandem duplication of a 55 kb region in the RPP5 locus that includes SNC1 and five other RPP5 locus R genes, through an apparent unequal crossing-over event. This dissertation also reports that the high frequency phenotypic suppression of the bal variant induced by mutagen treatment is associated with missense mutations in the SNC1 coding sequence that diminish or abolish SNC1 function. The results provide an example supporting the hypothesis that the clustered RPP5 locus R genes evolve by unequal crossing-over. Moreover, the data suggest that the RPP5 locus can adopt a metastable state highly susceptible to mutations that could facilitate the evolution of R genes in the locus.