抄録
We previously demonstrated that polyamines degraded by polyamine oxidase contribute to hypersensitive cell death by producing H2O2 during HR against tobacco mosaic virus infection. To further investigate relationships among polyamines, H2O2 and hypersensitive cell death, we employed tobacco cultured cells (BY2 cells). When BY2 cells were treated with cryptogein, an elicitor of HR, hypersensitive cell death was obvious. However, this was inhibited by α-difluoromethylornithine (DFMO), an inhibitor of ornithine decarboxylase. Polyamines were found to accumulate in apoplast of cryptogein-treated BY2 cells. In the presence of DFMO, however, such accumulation was almost suppressed. Polyamine oxidase activity was also detectable in apoplast. Generation of H2O2 was detected as early as 15 min after elicitation and this was also suppressed by the inhibitor, although effects were only apparent after 3 h or later. These results suggest that polyamines are a direct source of H2O2 in the late phase of HR.
