Sep. 18, 2006 Back-to-back scientific papers are offering a revolutionary look at the battlefield on which plant diseases are fought – and often lost – to bacteria.
The laboratory of Sheng Yang He at Michigan State University has changed the textbook description of a plant’s surface terrain and is unveiling new knowledge of how bacterial pathogens invade plants and take hold. The most recent paper, published in the Sept. 8 edition of Cell, redefines the role of the plant’s pores in defense against invading bacteria and how some bacteria can overpower plants.
Last month, in Science Magazine, the lab outlined a better understanding of how bacteria set up camp and destroy the plant’s ability to fight infection.
The work was funded by the National Institutes of Health and the U.S. Department of Energy and supported by the Michigan Agricultural Experiment Station.
“We’ve known for 100 years that bacterial pathogens cause illness in crops, yet we still don’t understand how they produce disease,” said He, a professor of plant biology, plant pathology, and microbiology and molecular genetics. “It’s very frustrating. How does this little thing do such great damage to plants?”
But this summer, Maeli Melotto, a research associate, and Bill Underwood, a graduate student, in He’s laboratory, shed light on the behavior of one the plant’s first lines of defense against disease. Pores called stomata are like tiny mouths that open and close during photosynthesis, exchanging gases. In sunshine, the stomata open. In darkness, they close to conserve water.
It has been assumed that these tiny ports were busy with their photosynthesis business and were merely unwitting doorways to invading bacteria on a plant’s surface. Melotto and Underwood, however, have discovered that stomata are an intricate part of the plant’s immune system that can sense danger and respond by shutting down.
The lab performed experiments on Arabadopsis, a common laboratory plant, but the mechanisms could be universal across all land plants.
“When we started looking more closely, and put bacteria on a plant surface, stomata close. It’s like they say ‘oh, we have to close the doors!’” Melotto said. “Even if it is in bright daylight, when the stomata are supposed to be open, they close.”
Some bacteria have gotten smarter. Melotto and Underwood found that plants recognized human-infecting bacteria, such as E. coli, and kept the stomata closed to them. Plant-infecting bacteria, like those most destructive to crops, have figured out a way to reopen the shut-down ports.
It appears those plant-based bacteria produce a phytotoxin, a chemical called coronatine, to force the pores back open. For bacteria, entry is crucial to causing disease and probably survival. They could die if left lingering on the surface. Animal-based bacteria do not produce coronatine.
“Now that we know a key step in bacteria’s attack, we have something we can learn to interfere with,” Melotto said. “From this we can learn about disease resistance.”
It’s a weighty issue. Bacterial diseases can be catastrophic to crops. One disease, called fire blight, did $40 million in destruction to Michigan apple trees in 2000 alone and all but eliminated commercial pear crops in Michigan for that year.
He also sees useful human health implications. Understanding that animal pathogens, like dangerous E. coli, cannot easily gain access inside the plant helps scientists know how to best combat bacteria that cause foodborne illness. It is important to know, he explained, whether foodborne illnesses rest on the surface of an edible plant, or nestle inside, impervious to washing.
“We are thinking about the mysteries of plant pathologies, but these have broad implications,” He said. “We haven’t understood very well how plants and bacteria interact, but we’re finally seeing the light.”
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