The plant immune response known as systemic acquired resistance (SAR) is a general defense mechanism that confers long-lasting resistance against a broad spectrum of pathogens. SAR triggers many molecular changes including accumulation of antimicrobial pathogenesis-related (PR) proteins. Transcription of PR genes in Arabidopsis is regulated by the coactivator NPR1 and the repressor SNI1. Pathogen infection also triggers an increase in somatic DNA recombination, which results in transmission of changes to the offspring of infected plants. However, it is not known how the induction of homologous recombination during SAR is controlled. Here, we show that SNI1 and RAD51D regulate both gene expression and DNA recombination. In a genetic screen for suppressors of sni1, we discovered that RAD51D is required for NPR1-independent PR gene expression. As a result, the rad51d mutant has enhanced disease susceptibility. Besides altered PR gene expression, rad51d plants are hypersensitive to DNA-damaging agents and are impaired in homologous recombination. The dual role of RAD51D and SNI1 in PR gene transcription and DNA recombination suggests a mechanistic link between the short-term defense response and a long-term survival strategy.
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