The NLR protein CbAR9 and the hydrolase CbSAHH form a module driving systemic acquired resistance against Colletotrichum in pepper.

Anthracnose, which is caused by fungal pathogens of the genus Colletotrichum, poses a substantial threat to global pepper (Capsicum spp.) production. However, the principal regulators and signaling pathways that mediate anthracnose resistance remain largely unknown. In this study, we demonstrate the roles of ANTHRACNOSE RESISTANCE 9 (CbAR9) and S-ADENOSYLHOMOCYSTEINE HYDROLASE (CbSAHH) in the methyl salicylate (MeSA) mobile signal activating systemic acquired resistance (SAR) in Capsicum baccatum. Phenotypic and molecular analyses showed that the nucleotide-binding domain and leucine-rich repeat protein CbAR9 enhances both local and systemic defense responses to Colletotrichum species through salicylic acid (SA)-dependent immunity, and it directly interacts with CbSAHH, a key enzyme in the methylation cycle. Knockdown of CbAR9 or CbSAHH significantly impaired SAR to Colletotrichum species. Moreover, the elevation of MeSA content and methylation capacity induced by Colletotrichum capsici in the primary infected leaves were compromised in CbAR9- and CbSAHH-silenced plants. Notably, MeSA treatment in the primary infected leaves restored the diminished SAR to C. capsici in CbAR9- and CbSAHH-silenced plants. These findings show that the CbAR9-CbSAHH module contributes SAR to Colletotrichum species through activating the MeSA mobile signal.