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Critical early-defense trigger in plants found

ITHACA, N.Y. -- The gene for an enzyme that is key to natural disease resistance in plants has been discovered by biologists at the Boyce Thompson Institute for Plant Research (BTI) and at Cornell University. The researchers say that by enhancing the activity of the enzyme they might be able to boost natural disease resistance in crop plants without resorting to pesticides or the introduction of non-plant genes.

The research, reported in the latest (May 16) issue of the journal Cell , describes the discovery of the gene that codes for an enzyme (a protein that carries out a chemical reaction) that is activated when a plant senses it is being attacked by a pathogen. When activated, the enzyme produces nitric oxide (NO), a hormone that tells the plant to turn on its defense arsenal.

According to plant pathologist Daniel F. Klessig, lead author of the Cell paper and president of BTI, located on the Cornell campus, the discovery provides a new understanding of the biochemical and genetic pathways in plants that enable them to protect themselves from disease.

"It's known that the hormone nitric oxide plays an important role in immunity in plants as well as in humans and other animals," says Klessig. "But the enzyme responsible for its production in plants was unknown until now. With this discovery, we may be able to modify plants so that they produce nitric oxide more quickly, or in larger amounts, when they are attacked by a disease-causing pathogen, enabling them to better protect themselves from invaders."

Authors of the Cell paper, "The Pathogen-Inducible Nitric Oxide Synthase (iNOS) in Plants is a Variant of the P Protein of the Glycine Decarboxylase Complex," also include Meena Chandok, a BTI senior research associate; Anders Jimmy Ytterberg, Cornell doctoral candidate in plant biology; and Klaas J. van Wijk, Cornell assistant professor of plant biology.

"This discovery really is a surprise because the plant enzym
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Contact: David Brand
deb27@cornell.edu
607-255-3651
Cornell University News Service
15-May-2003


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