Systemic acquired resistance (SAR), an inducible plant-defense response to local infection, requires the signaling molecule salicylic acid (SA) and the transcriptional coactivator NPR1, with concerted activation of pathogenesis-related (PR) genes. Arabidopsis sni1 is an npr1 suppressor and derepression of defense genes in sni1 causes reduced growth and fertility and increased homologous recombination. Characterizing suppressors of sni1, we identify the DNA damage repair proteins SSN2 and RAD51D as genetic and physical interactors with SNI1. During plant defense, SSN2 and possibly RAD51D replace the transcription repressor SNI1 at pathogenesis-related gene promoters. In the presence of SNI1, NPR1 is also required for SSN2 binding. Thus, coordinated action of SNI1, SSN2-RAD51D, and NPR1 ensures the tight control of plant immune gene expression. Given that the SSN2-RAD51D complex is conserved in eukaryotes, their dual function in homologous recombination and transcription regulation of plant-defense genes suggests a general link between these two stress responses.