PDF(Pubmed)
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.
摘要：
雷帕霉素靶蛋白（TOR）调节与植物生长相关的基本过程，发展,和细胞死亡通过调节代谢活动和翻译响应环境信号。ATP竞争性TOR抑制剂AZD8055抑制了感染了不相容的青枯病菌的本氏烟草的超敏反应（HR）细胞死亡。HR标记基因hin1的诱导表达也被AZD8055处理抑制。为了进一步阐明TOR调节HR细胞死亡的潜在机制，我们专注于TOR相关的ErbB3结合蛋白1（EBP1）。我们在N.benthamiana基因组中发现了四个EBP1直向同源物。所有四种EBP1直向同源物的表达水平均被蓝枯菌感染上调。四个NbEBP1直系同源物的沉默抑制了HR细胞死亡的诱导，hin1表达式,和活性氧的产生。这些结果表明，TOR信号通路有助于调节HR细胞的死亡以及与活性氧相关的信号。
