Abstract
Boron (B) cross-links pectic polysaccharides at the rhamnogalacturonan II regions and thereby contributes to build the cell wall. However, it remains unknown how B deficiency triggers various metabolic disorders and brings about cell death. To understand this mechanism, we have analyzed the responses of cultured tobacco BY-2 cells under B deficiency.
When 3-day-old cells were transferred to a B-free medium, dead cells started to increase from 24 h after the treatment. We previously showed that the genes for antioxidative enzymes are upregulated in low B-acclimated cells, which suggests that oxidative damages are involved in low B stress. In the present study we found that lipid peroxides accumulated in -B cells by 18 h, prior to the increase in the dead cell population. In addition, an antioxidant butylated hydroxyanisole reduced cell death. These results indicate that oxidative damage does occur under B deficiency as the direct cause of cell death.
