Suppressed expression of ErbB3-binding protein 1 (EBP1) genes compromised the hypersensitive response cell death in Nicotiana benthamiana.

Abstract

Target of rapamycin (TOR) regulates essential processes associated with plant growth, development, and cell death by modulating metabolic activities and translation in response to environmental signals. The ATP-competitive TOR inhibitor AZD8055 suppressed the hypersensitive response (HR) cell death in Nicotiana benthamiana infected with the incompatible Ralstonia solanacearum. The induced expression of the HR marker gene hin1 was also inhibited by the AZD8055 treatment. To further clarify the mechanisms underlying TOR-regulated HR cell death, we focused on TOR-related ErbB3-binding protein 1 (EBP1) in N. benthamiana (NbEBP1). We found four EBP1 orthologs in the N. benthamiana genome. The expression levels of all four EBP1 orthologs in N. benthamiana were up-regulated by the R. solanacearum infection. The silencing of the four NbEBP1 orthologs suppressed the induction of HR cell death, hin1 expression, and the production of reactive oxygen species. These results suggest that the TOR signaling pathway helps regulate HR cell death along with reactive oxygen species-related signaling in N. benthamiana.