Dissection of Arabidopsis Bax inhibitor-1 suppressing Bax-, hydrogen peroxide-, and salicylic acid-induced cell death

• Published in: The Plant cell 2004-01, Vol.16 (1), p.21-32
• Main Authors: Kawai-Yamada, M, Ohori, Y, Uchimiya, H
• Format: Article
• Language: English
• Subjects: Adaptation, Physiological - drug effects; Adaptation, Physiological - genetics; Amino Acid Sequence; Amino acids; Apoptosis; Apoptosis - drug effects; Apoptosis - genetics; Arabidopsis - genetics; Arabidopsis - growth & development; Arabidopsis Proteins - genetics; Arabidopsis Proteins - metabolism; Arabidopsis thaliana; Bax Inhibitor-1 gene; bcl-2-Associated X Protein; Cell death; Cell Line; Cell lines; cell suspension culture; Gene Expression Regulation, Developmental; Gene Expression Regulation, Plant; gene overexpression; Hydrogen peroxide; Hydrogen Peroxide - pharmacology; Ion Channels - antagonists & inhibitors; Ion Channels - physiology; Membrane Proteins - genetics; Membrane Proteins - metabolism; messenger RNA; metabolic inhibitors; Molecular Sequence Data; Mortality; Nicotiana tabacum; Oxidative stress; Oxygen - metabolism; Plant cells; plant proteins; Plants; Plants, Genetically Modified; Proteins; Proto-Oncogene Proteins - genetics; Proto-Oncogene Proteins - metabolism; Proto-Oncogene Proteins c-bcl-2; reactive oxygen species; Reactive Oxygen Species - metabolism; RNA, Messenger - drug effects; RNA, Messenger - genetics; RNA, Messenger - metabolism; salicylic acid; Salicylic Acid - pharmacology; Sequence Homology, Amino Acid; stress tolerance; superoxide anion; transcription (genetics); Transgenic plants; Yeasts
• ISSN: 1040-4651; 1532-298X
• DOI: 10.1105/tpc.014613

Overexpression of plant Bax Inhibitor-1 (BI-1) was able to suppress Bax-mediated cell death in yeast and Arabidopsis. Here, we demonstrate that reactive oxygen species production induced by the ectopic expression of Bax was insensitive to the coexpression of AtBI-1. Similarly, H2O2- or salicylic acid-mediated cell death also was suppressed in tobacco BY-2 cells overexpressing AtBI-1. To define the functional domain of AtBI-1 as a cell death suppressor, a truncated series of the AtBI-1 protein was analyzed in yeast possessing a galactose-inducible mammalian Bax. The results showed that C-AtBI-1 (with the C-terminal 14 amino acids deleted) lost the ability to sustain cell growth. Furthermore, a mutant protein in which the C-terminal seven amino acid residues of AtBI-1 were replaced with others lacking a coiled-coil structure failed to inhibit cell death, suggesting that the C-terminal region is essential for the inhibition of cell death. We also noted that the C-terminal hydrophilic region was interchangeable between animal and plant Bax inhibitors.