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

• Published in: Physiological and molecular plant pathology Vol. 116; p. 101724
• Main Authors: Ueta, Yukiko, Mizutani, Yuka, Ohnishi, Kouhei, Hikichi, Yasufumi, Kiba, Akinori
• Format: Journal Article
• Language: English
• Published: Elsevier Ltd 01.12.2021
• Subjects: Hypersensitive response; Jasmonic acid; Nicotiana benthamiana; Phosphatidylinositol-phospholipase C1; Ralstonia solanacearum; Salicylic acid; Salicylic acid; Nicotiana benthamiana; Hypersensitive response; Ralstonia solanacearum; Jasmonic acid; Phosphatidylinositol-phospholipase C1
• ISSN: 0885-5765; 1096-1178
• DOI: 10.1016/j.pmpp.2021.101724

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. •The article showed the negative regulation of hypersensitive response by phosphoinositide-specific phospholipase C1.