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Trio of plant genes prevent ’too many mouths’

08.07.2005

Keiko Torii holds a mutated version – one that’s an inch tall and covered densely with microscopic stomata – and a normal plant of Arabidopsis, a small flowering plant that is widely used as a model organism in plant biology.
Photo credit: University of Washington

A signaling pathway required for plants to grow to their normal size appears to have an unexpected dual purpose of keeping the plant from wallpapering itself with too many densely clustered stomata.

"It’s surprising that size and stomata patterning – both key to plants being able to survive on dry land – are using the same signaling components," says Jessica McAbee, a University of Washington research associate in biology. She’s one co-author of a report in the July 8 issue of Science about work with Arabidopsis, a weed-like member of the crucifer family for which scientists already have a genomic map.

Stomata are microscopic pores on the surface of plants that open to allow plants to take in carbon dioxide from the air for photosynthesis. They close when there is the danger that the plant tissue may lose too much moisture.

"Specialized cells open and close the stomata, much like opening and closing a mouth," says Keiko Torii, UW assistant professor of biology. Stomata too close together can’t operate effectively.

Understanding the mechanisms that control stomata patterning offers insights into such questions as how plants evolved to protect themselves when they moved from water to land, Torii says. Even atmospheric scientists are interested in such basic plant biology, given the enormous amount of the greenhouse gas carbon dioxide taken up by the Earth’s plants.

Scientists already believed that part of the signaling pathway for stomata production included the receptor-like protein Too Many Mouths, so called because when absent the plant makes too many stomata, or mouths.

Scientists were searching for a single stomata gene that had to be working in concert with Too Many Mouths to get an efficient distribution of stomata, Torii says. No one was considering that more than one gene could be involved, much less three, or that the genes could be serving other purposes, she says.

The UW team of four female scientists serendipitously discovered what appears to be part of the pathway that tempers the production of stomata while studying a trio of genes that code for signaling receptors required for normal plant height.

The scientists were working on a basic understanding of plant growth as part of U.S. Department of Energy and Japanese Science and Technology Agency-funded work about growing plant material, or biomass, suitable for producing fuel. By mutating all three genes – essentially putting them all out of action – the researchers got dwarf plants an inch high instead of the normal 1½ feet. Surprisingly the plants also were so densely covered with stomata that most stomata were touching each other.

These genes appear to have roles at two points in the production of stomata. First, they inhibit undifferentiated cells – those unspecialized cells that have yet to turn into specific cell types – from making too many stomata and then they repress the development of two guard cells that open and close the stomata pore.

Co-authors of the Science paper besides Torii and McAbee are lead author Elena Shpak, former research associate at the UW and starting this fall as an assistant professor at California State University, Fullerton, and Lynn Pillitteri, a UW research associate in biology.