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Light and oxygen are not required for harpin-induced cell death

Lookup NU author(s): Simon Driscoll, Professor Christine Foyer

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Abstract

Nicotiana sylvestris leaves challenged by the bacterial elicitor harpin NEa were used as a model system in which to determine the respective roles of light, oxygen, photosynthesis, and respiration in the programmed cell death response in plants. The appearance of cell death markers, such as membrane damage, nuclear fragmentation, and induction of the stress-responsive element Tnt1, was observed in all conditions. However, the cell death process was delayed in the dark compared with the light, despite a similar accumulation of superoxide and hydrogen peroxide in the chloroplasts. In contrast, harpin-induced cell death was accelerated under very low oxygen (〈0.1% O2) compared with air. Oxygen deprivation impaired accumulation of chloroplastic reactive oxygen species (ROS) and the induction of cytosolic antioxidant genes in both the light and the dark. It also attenuates the collapse of photosynthetic capacity and the respiratory burst driven by mitochondrial alternative oxidase activity observed in air. Since alternative oxidase is known to limit overreduction of the respiratory chain, these results strongly suggest that mitochondrial ROS accumulate in leaves elicited under low oxygen. We conclude that the harpin-induced cell death does not require ROS accumulation in the apoplast or in the chloroplasts but that mitochondrial ROS could be important in the orchestration of the cell suicide program. © 2007 by The American Society for Biochemistry and Molecular Biology, Inc.


Publication metadata

Author(s): Garmier M, Priault P, Vidal G, Driscoll S, Djebbar R, Boccara M, Mathieu C, Foyer CH, De Paepe R

Publication type: Article

Publication status: Published

Journal: Journal of Biological Chemistry

Year: 2007

Volume: 282

Issue: 52

Pages: 37556-37566

ISSN (print): 0021-9258

ISSN (electronic): 1083-351X

Publisher: American Society for Biochemistry and Molecular Biology, Inc.

URL: http://dx.doi.org/10.1074/jbc.M707226200

DOI: 10.1074/jbc.M707226200

PubMed id: 17951254


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