Sep. 3, 1999 WEST LAFAYETTE, Ind. -- A Purdue University researcher has discovered that a natural plant toxin can stop invading fungi by turning a fungus's protein production system against itself. The findings, will be announced Monday (9/6) by horticulture Professor Ray Bressan at the meeting of the Chinese National Academy of Sciences in Shanghai, could lead to genetically engineered crops that are able to resist fungal infections.
"The plant toxin tricks fungal cells into committing suicide," Bressan says. "It works by inducing programmed cell death."
Programmed cell death, also called apoptosis, is a process that plants and animals use during development and for protection. For example, cells in a human fetus' developing ball of hand tissue die by apoptosis to create the spaces between fingers. Also, if sun exposure damages the DNA of a person's skin cells, those cells often kill themselves so that they won't become cancerous. Certain promising anti-cancer compounds under study work by causing apoptosis of cancer cells.
Osmotin, the plant toxin Bressan worked with, is one of several chemicals that plants produce to fight off fungal invasions. To see how osmotin worked, Bressan tested it against yeast.
While yeast isn't a plant pathogen, it is a fungus that's both easy to work with and well understood. Also, in interactions with osmotin, yeast acts the same as fungi that invade plants.
Bressan added osmotin to a culture of yeast cells, just as a plant naturally would send the compound out to fend off an attacking fungus. Defensive proteins in the yeast cell walls caught and stopped some osmotin molecules, but not all. Some got through, chewed holes in the cell membranes and made them leak.
This part of osmotin's mode of action wasn't too surprising, because many other disease-fighting compounds act similarly in plants. But osmotin did more than chew holes in membranes.
It also altered the protein-generating machinery of the fungal cells, causing the fungus to build weaker walls, Bressan found. Osmotin was telling the fungus to tear down its defenses and let in more osmotin -- and the fungus did it.
In other words, osmotin caused fungal cells to undergo apoptosis, to program their own death.
Using genetic engineering, researchers may use this information to beef up the plant defenses that cause apoptosis in fungi.
"If it's true, this gives us possibilities for engineering more potent antifungal compounds," says John Duvick, research coordinator for disease resistance in the Department of Crop Protection at Pioneer Hi-Bred International. "We could find a protein or molecule that does the job better than the ones we now have."
And if researchers can genetically engineer crops to better resist fungi, farmers will spray fewer fungicides. That would save them money and reduce the amount of pesticides in the environment. Plant diseases -- many of them fungal diseases -- still cause more that $9 billion in annual losses in the United States, according Roy E. Gingery, a program leader for the U.S. Agricultural Research Service's National Program in Plant Diseases.
For his research, Bressan won Purdue's 1999 Herbert Newby McCoy award.
"Bressan's research is an excellent example of the payoff that comes from discovery in basic science," says Randy R. Woodson, director of Purdue Agricultural Research Programs. "This discovery led his group to develop novel approaches to control diseases in plants. Discoveries in this area will continue to provide farmers with new technologies for the control of plant disease."
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