Phosphatidylinositol-phospholipase C3 negatively regulates the hypersensitive response via complex signaling with MAP kinase, phytohormones and reactive oxygen in Nicotiana benthamiana.

Abstract

Phospholipid signaling plays important roles in plant immune responses. Here, we focused on two phospholipase C3 (PLC3) orthologs in the Nicotiana benthamiana genome, NbPLC3-1 and NbPLC3-2. We created NbPLC3-1 and NbPLC3-2-double-silenced plants (NbPLC3s-silenced plants). In NbPLC3s-silenced plants challenged with Ralstonia solanacearum 8107, the induction of the hypersensitive response (HR), including HR-related cell death and bacterial population reduction, was accelerated, the expression level of Nbhin1, an HR marker gene was enhanced, the expression levels of genes involved in salicylic acid and jasmonic acid signaling drastically increased, the reactive oxygen species hyper-production, was accelerated, and NbMEK2-induced HR-related cell death were also enhanced. Accelerated HR-cell death was also observed by bacterial pathogens Pseudomonas cichorii and P. syringae and bacterial AvrA, oomycete INF1 and TMGMV-CP with L1 in NbPLC3s-silenced plants. Although HR-related cell death was accelerated, the bacterial population was not reduced in double NbPLC3s and NbCoi1 suppressed plants nor in NbPLC3s-silenced NahG plants. The HR-related cell death acceleration and bacterial population reduction resulting from NbPLC3s-silencing were compromised by the concomitant suppression of either NbPLC3s and NbrbohB or NbPLC3s and NbMEK2. Thus, NbPLC3s may negatively regulate both HR-related cell death and disease resistance through MAP kinase- and reactive oxygen species-dependent signaling. Disease resistance was also regulated by NbPLC3s through jasmonic acid- and salicylic acid-dependent pathways.