Phosphatidylinositol-phospholipase C1 negatively regulates the hypersensitive response in Nicotiana benthamiana

Phospholipid signaling plays an important role in plant immune responses. Here, we isolated two phospholipase C1 (PLC1) orthologs in the N. benthamiana genome, designated N. benthamiana PLC1-1 and PLC1-2 (NbPLC1-1 and NbPLC1-2). The NbPLC1-2-silenced plants showed an accelerated hypersensitive response (HR) challenged with an incompatible strain of R. solanacearum. Additionally, accelerated hypersensitive cell death was also observed in The NbPLC1-2-silenced plants by the bacterial effectors AvrA and PopA1 and oomycete INF1. Expression of NbPR-1, a marker gene for salicylic acid signaling, and NbPR-4, a marker gene for jasmonic acid signaling, was drastically increased by incompatible R. solanacearum in the NbPLC1-2-silenced plants. Although HR cell death was accelerated, the bacterial population was not reduced in the NbPLC1-2-silenced NahG plants compared to the NbPLC1-2-silenced wild type N. benthamiana plants. The hypersensitive cell death acceleration and bacterial population reduction from the NbPLC1-2 silencing was compromised by concomitant suppression of the NbPLC1-2 with NbCoi1. These results suggested that the NbPLC1-2 might act as a negative regulator for the HR in N. benthamiana. The NbPLC1-2 protein might negatively regulate both cell death and disease resistance via jasmonic acid-dependent signaling and suppress disease resistance via a salicylic acid-dependent pathway.