Abstract
Reactive oxygen species (ROS) generated by biotic and abiotic stresses act as messenger molecules in stress adaptation and programmed cell death. Overexpression of Arabidopsis Bax inhibitor-1 (AtBI-1), ER membrane protein exist in a wide range of organisms, suppresses hydrogen peroxide-, SA-, and elicitor-induced plant cell death. Expression of BI-1 gene is rapidly up-regulated during wounding and pathogen attack, but down-regulated by elicitor induced HR. Furthermore, AtBI-1 overexpressing and knock-down plants grow normally, suggesting the involvement of AtBI-1 in ROS-mediated stress response, but not in developmental PCD. Calmodulin (CaM) and cytochrome b5 (Cb5) were isolated as BI-1 interactants. The C-terminal mutants of AtBI-1, which lacked the cell death suppression activity, failed to bind with CaM, indicating such interaction would be necessary for the suppressive action of AtBI-1. Furthermore, AtBI-1 was supposed to interact with FAH via Cb5, suggesting possible involvement of sphingolipid metabolism in plant cell death regulation.
