Bax-induced cell death in tobacco is similar to the hypersensitive response

• Published in: Proceedings of the National Academy of Sciences - PNAS 1999-07, Vol.96 (14), p.7956-7961
• Main Authors: Lacomme, C, Santa Cruz, S
• Format: Article
• Language: English
• Subjects: Animals; Apoptosis; bcl-2-Associated X Protein; Biological Sciences; carboxylic acids; Cell death; Cellular biology; comparisons; Complementary DNA; defense mechanisms; deletions; disease resistance; experimental infections; Flowers & plants; Genes; Green Fluorescent Proteins; Infections; Leaves; Lesions; Luminescent Proteins - genetics; Mice; Microscopy, Confocal; Mitochondria; Mitochondria - drug effects; Mitochondria - physiology; Mitochondria - ultrastructure; mutants; n gene; Nicotiana; Nicotiana - cytology; Nicotiana - physiology; Nicotiana benthamiana; nicotiana edwardsonii; Nicotiana tabacum; Nucleocapsid Proteins - genetics; Nucleocapsid Proteins - physiology; okadaic acid; Okadaic Acid - pharmacology; pathogenesis-related proteins; Phenotype; Plant cells; plant proteins; Plants; Plants, Toxic; protein synthesis; Proteins; Proto-Oncogene Proteins - genetics; Proto-Oncogene Proteins - physiology; Proto-Oncogene Proteins c-bcl-2; Tobacco; Tobacco mosaic virus; Tobacco Mosaic Virus - genetics; Tobacco Mosaic Virus - physiology; Transcription, Genetic; transgenic plants; Viruses; Yeasts
• ISSN: 0027-8424; 1091-6490
• DOI: 10.1073/pnas.96.14.7956

Bax, a death-promoting member of the Bcl-2 family of proteins, triggered cell death when expressed in plants from a tobacco mosaic virus vector. Analysis of Bax deletion mutants demonstrated a requirement for the BH1 and BH3 domains in promoting rapid cell death, whereas deletion of the carboxyl-terminal transmembrane domain completely abolished the lethality of Bax in plants. The phenotype of cell death induced by Bax closely resembled the hypersensitive response induced by wild-type tobacco mosaic virus in tobacco plants carrying the N gene. The cell death-promoting function of Bax in plants correlated with accumulation of the defense-related protein PR1, suggesting Bax activated an endogenous cell-death program in plants. In support of this view, both N gene- and Bax-mediated cell death was blocked by okadaic acid, an inhibitor of protein phosphatase activity. The ability of Bax to induce cell death and a defense reaction in plants suggests that some features of animal and plant cell death processes may be shared.