Abstract
The molecular links between cell cycle control and the regulation of programmed cell death are largely unknown in plants. Using synchronized tobacco BY-2 cells, we analyzed the cell-cycle dependence of elicitor-induced defense responses. A proteinaceous elicitor, cryptogein, induced cell cycle arrest at the G1 and G2 phases prior to the hypersensitive cell death (Plant J. (2004) 40: 131-142). Cryptogein treatment during the G1 or S phases induced biphasic responses in activation of MAP kinases and ROS production. In contrast, that during the G2 or M phases induced only rapid and transient phase, suggesting that although cryptogein recognition occurred at all phases, only the recognition during the S or G1 phases induces the prolonged MAPKs activation and the prolonged ROS production, followed by cell cycle arrest and cell death. Elicitor signal transduction depends on the cell cycle and is differently regulated at each phase.
