Abstract
Priming of defense increases the responsiveness of the plant immune system and can provide broad-spectrum protection against disease. Recent evidence suggests that priming of defense can be inherited epigenetically to following generations. However, the mechanisms of long-lasting defense priming within one generation remains poorly understood. Here, we have investigated the mechanistic basis of long-lasting induced resistance after treatment with β -aminobutyric acid (BABA), an agent that mimics biologically induced resistance phenomena. BABA-induced resistance (BABA-IR) is based on priming of salicylic acid (SA)-dependent and SA-independent defenses. BABA-IR could be detected up to 28 days after treatment of wild-type Arabidopsis. This long-lasting component of the induced resistance response requires the regulatory protein NPR1 and is associated with priming of SA-inducible genes. In contrast, NPR1-independent resistance by BABA was transient and had disappeared by 14 days after treatment. Chromatin immunoprecipitation (ChIP) assays revealed no increased acetylation of histone H3K9 at promoters regions of priming-responsive genes, indicating that this post-translational histone modification is not critical for long-term transcriptional priming. Interestingly, the kyp-6 mutant, which is affected in methyltransferase activity of H3K9, was blocked in long-lasting BABA-IR, indicating a critical requirement of this post-translational histone modification in long-lasting BABA-IR. Considering that KYP suppresses gene transcription through methylation of H3K9 and CpHpG DNA methylation, we propose that KYP enables long-term defense gene priming by silencing suppressor genes of SA/NPR1-dependent genes.