Arabidopsis Bax inhibitor‐1 functions as an attenuator of biotic and abiotic types of cell death

Summary Programmed cell death (PCD) is a common process in eukaryotes during development and in response to pathogens and stress signals. Bax inihibitor‐1 (BI‐1) is proposed to be a cell death suppressor that is conserved in both animals and plants, but the physiological importance of BI‐1 and the impact of its loss of function in plants are still unclear. In this study, we identified and characterized two independent Arabidopsis mutants with a T‐DNA insertion in the AtBI1 gene. The phenotype of atbi1‐1 and atbi1‐2 , with a C‐terminal missense mutation and a gene knockout, respectively, was indistinguishable from wild‐type plants under normal growth conditions. However, these two mutants exhibit accelerated progression of cell death upon infiltration of leaf tissues with a PCD‐inducing fungal toxin fumonisin B1 (FB1) and increased sensitivity to heat shock‐induced cell death. Under these conditions, expression of AtBI1 mRNA was up‐regulated in wild‐type leaves prior to the activation of cell death, suggesting that increase of AtBI1 expression is important for basal suppression of cell death progression. Over‐expression of AtBI1 transgene in the two homozygous mutant backgrounds rescued the accelerated cell death phenotypes. Together, our results provide direct genetic evidence for a role of BI‐1 as an attenuator for cell death progression triggered by both biotic and abiotic types of cell death signals in Arabidopsis .