EDS1-Dependent Cell Death and the Antioxidant System in Leaves is Deregulated by the Mammalian Bax.

Cell death is the ultimate end of a cell cycle that occurs in all living organisms during development or responses to biotic and abiotic stresses. In the course of evolution, plants and animals evolve various molecular mechanisms to regulate cell death; however, some of them are conserved among both these kingdoms. It was found that mammalian proapoptotic BCL-2 associated X (Bax) protein, when expressed in plants, induces cell death, similar to hypersensitive response (HR). It was also shown that changes in the expression level of genes encoding proteins involved in stress response or oxidative status regulation mitigate Bax-induced plant cell death. In our study, we focused on the evolutional compatibility of animal and plant cell death molecular mechanisms. Therefore, we studied the deregulation of reactive oxygen species burst and HR-like propagation in expressing mammalian Bax. We were able to diminish Bax-induced oxidative stress and HR progression through the genetic cross with plants mutated in (), which is a plant-positive HR regulator. Plants expressing the mouse Bax gene in null mutant background demonstrated less pronounced cell death and exhibited higher antioxidant system efficiency compared to Bax-expressing plants. Moreover, /Bax plants did not show HR marker genes induction, as in the case of the Bax-expressing line. The present study indicates some common molecular features between animal and plant cell death regulation and can be useful to better understand the evolution of cell death mechanisms in plants and animals.