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 longlasting
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.
CORE (COnnecting REpositories)
CORE (COnnecting REpositories)