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Expression of the Baculovirus p35 Protein in Tobacco Affects Cell Death Progression and Compromises N Gene-Mediated Disease Resistance Response to Tobacco mosaic virus

June 2003 , Volume 16 , Number  6
Pages  485 - 494

Olga del Pozo and Eric Lam

1Biotech Center, Foran Hall, 59 Dudley Road, Rutgers State University of New Jersey, New Brunswick, NJ 08903, U.S.A.

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Accepted 31 December 2002.

The p35 protein from baculovirus is a broad-range caspase inhibitor and suppresses programmed cell death in animals. We report here the effects of transgenic expression in tobacco of the p35 protein during the hypersensitive response (HR). Expression of p35 causes partial inhibition of nonhost HR triggered by bacteria and gene-for-gene HR triggered by virus. Infection of p35-expressing tobacco plants with Tobacco mosaic virus (TMV) disrupts N-mediated disease resistance, causing systemic spreading of the virus within a resistant background. Mutant variants altered in aspartate residues within the loop region of p35 are inefficient substrates for caspases in vitro, and they do not suppress caspase proteolytic activity in animal systems. Tobacco plants expressing these mutant variants of the p35 protein do not show inhibition of HR cell death or enhanced virus systemic movement. Thus, HR inhibition and TMV systemic spreading phenotype in p35-expressing plants correlate with the ability of the p35 protein to suppress caspase activity in animal systems. In addition, a C-terminal truncated variant of p35 is unable to suppress cell death in animals as well as HR cell death in transgenic tobacco. Our results provide evidence for the participation of caspase-like proteases during the HR. In addition, they suggest that timely activation of cell death is necessary for effective TMV containment within the primary infection site.

Additional keywords: caspase-like proteins.

© 2003 The American Phytopathological Society