Explaining how ozone "chokes up" plants

December 05, 1999

University Park, Pa. --- Penn State researchers have identified how ozone, a major smog constituent, affects the microscopic breathing pores on plants' leaves, a process that may figure in the estimated $3 billion in agricultural losses caused by ozone air pollution in the U.S. each year.

Dr. Gro Torsethaugen, a postdoctoral researcher in Penn State's Environmental Resources Research Institute, says, "Although elevated ground levels of ozone resulting from traffic and other fossil fuel burning have long been associated with losses in agricultural yield, the precise cellular targets of ozone's action were essentially unknown. Our work has shown, for the first time, that, rather than causing the pores or stomates on a plant's leaves to close, as was generally assumed, ozone actually inhibits stomatal opening by directly affecting the 'guard cells' that control the opening."

Torsethaugen adds that knowing ozone's specific cellular targets may make it possible in the future to breed or to genetically engineer new plant varieties to improve productivity in geographic regions, such as California, with significant ozone exposure.

Torsethaugen and her co-authors Dr. Eva J. Pell, the Steimer professor of agricultural sciences, and Dr. Sarah M. Assmann, professor of biology, published their findings in a recent issue of the Proceedings of the National Academy of Sciences (PNAS).

Plants take in the carbon dioxide they need for photosynthesis through their stomates, Torsethaugen explains. They also release oxygen made in photosynthesis through the same pores. Ozone can also enter the plant through the stomates and can affect photosynthesis via that route. The Penn State experiments point to direct action on the guard cells as an additional path that ozone takes to decrease carbon dioxide assimilation and reduce plant productivity.

Torsethaugen conducted the experiments with fava bean plants, an important world food source and a species scientists favor for guard cell studies. Using various techniques, she examined the pores on the leaves of whole plants and portions of leaf surfaces and then studied the isolated guard cells.

In whole plants and the leaf surfaces, she found that ozone directly affects the stomatal opening.

Using isolated guard cells, she monitored the flow of potassium, in a positively charged or ion form, into and out of the cells.

"We monitored potassium because it is a major component in the osmotic process," she says. "If the potassium ion concentration is increased, water comes into the cell by osmosis and the guard cells surrounding the stomate swell. This swelling causes the pore to open."

Ozone exposure reduced the flow of potassium ions into the guard cells but did not affect the outward flow, indicating that ozone inhibits the opening of the pores.

In their PNAS paper, the authors note that their findings may have particular relevance during drought. They write, "Stomatal closure during a period of drought may be less readily reversed in ozone-exposed plants. This may be particularly relevant because the highest ozone concentrations are sometimes associated with times of drought."

In addition, they write "In major agricultural regions with high light environments and significant ozone exposure - e.g. the "South Coast Air Basin of California, which has the most extreme ozone levels in the U.S. - midday stomatal closure often occurs because of the low ambient humidity that results from the high light, high temperature conditions of midday. Because the generation of ozone in photochemical smog depends on high solar irradiation, ozone inhibition of stomatal opening could significantly retard stomatal reopening in the afternoon after this mid-day depression and consequently reduce crop yield."

Identification of the potassium ion channel as a target for ozone action opens the door to selectively breeding or genetically engineering less ozone sensitive plants to improve plant productivity in geographic regions with significant ozone expose.

However, the Penn State researchers also note that "Our identification of a specific ion channel as a target for ozone action may prompt comparable studies in mammalian system, leading to improved understanding of and treatment for the disease etiologies exacerbated by ozone. "

The research was supported in part by a grant from the Binational Agricultural Research and Development/U.S. Department of Agriculture. The Department of Biology, University of Oslo, Norway, where Torsethaugen earned her doctorate, provided additional support.
EDITORS: Dr. Torsethaugen is at 814-865-0680 or gxt6@psu.edu by email.

Penn State

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