NpSKP1-1A enhances Nicotiana plants resistance to black shank disease through the jasmonic acid biosynthesis pathway and is positively regulated by NpWRKY2.

Black shank disease, caused by Phytophthora parasitica var. Nicotianae (P. nicotianae), severely affects the quality and yield of Nicotiana plants. Although resistance genes from some wild Nicotiana plant species, such as Nicotiana plumbaginifolia, were transferred to cultivated Nicotiana plant long ago, the underlying molecular mechanisms remain unclear. In previous work, NpSKP1-1A was found to interact with NpPP2-B10, which positively regulates Nicotiana plants resistance to P. nicotianae. In this study, we investigated the roles of NpSKP1-1A in resistance to P. nicotianae in Nicotiana plants. First, RT-qPCR and GUS assay results demonstrated that P. nicotianae infection induces an increase in NpSKP1-1A expression. Second, NpSKP1-1A was confirmed to positively regulate Nicotiana plants resistance to P. nicotianae through VIGS experiment in N. plumbaginifolia and heterologous overexpression in the susceptible Nicotiana plants cultivar Honghua Dajinyuan. Third, transcriptome data, LC-MS analysis, and VIGS experiments indicated that the jasmonic acid (JA) pathway is involved in N. plumbaginifolia resistance to P. nicotianae. Fourth, RT-qPCR and LC-MS analyses showed that NpSKP1-1A promotes JA biosynthesis. Y2H and BiFC assays further demonstrated that NpSKP1-1A interacts with NtCOI1 and NtCullin1 to form the SCFCOI1 complex, which participates in JA signal transduction. Finally, results of further analyses showed that NpWRKY2 performed positive regulatory effect on NpSKP1-1A. This study suggests that NpSKP1-1A positively modulates JA signaling, thereby boosting Nicotiana plants resistance against P. nicotianae. Understanding this regulatory module could provide valuable insights for improving Nicotiana plants resistance to P. nicotianae.