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THE PLANT CELL, Vol 8, Issue 11 1991-2001, Copyright © 1996 by American Society of Plant Biologists
Inhibition of Programmed Cell Death in Tobacco Plants during a Pathogen-Induced Hypersensitive Response at Low Oxygen Pressure
R. Mittler, V. Shulaev, M. Seskar and E. Lam
Center for Agricultural Molecular Biology, Foran Hall, Dudley Road, Rutgers, The State University of New Jersey, Cook College, P.O. Box 231, New Brunswick, New Jersey 08903-0231
The hypersensitive response (HR) of plants to invading pathogens is thought
to involve a coordinated activation of plant defense mechanisms and
programmed cell death (pcd). To date, little is known about the mechanism
underlying death of plant cells during this response. In addition, it is
not known whether suppression of pcd affects the induction of other defense
mechanisms during the HR. Here, we report that death of tobacco cells
(genotype NN) infected with tobacco mosaic virus (TMV) is inhibited at low
oxygen pressure. In contrast, virus replication and activation of defense
mechanisms, as measured by synthesis of the pathogenesis-related protein
PR-1a, were not inhibited at low oxygen pressure. Bacterium-induced pcd was
also inhibited at low oxygen pressure. However, pcd induced by TMV or
bacteria was not inhibited in transgenic tobacco plants expressing the
mammalian anti-pcd protein Bcl-XL. Our results suggest that ambient oxygen
levels are required for efficient pcd induction during the HR of plants and
that activation of defense responses can be uncoupled from cell death.
Furthermore, pcd that occurs during the interaction of tobacco with TMV or
bacteria may be distinct from some cases of pcd or apoptosis in animals
that are insensitive to low oxygen or inhibited by the Bcl-XL protein.
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