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ANN ARBOR—University of Michigan scientist Steven Clark has taken a major step toward understanding one of life’s oldest mysteries—how genes work together in plants to turn generic cells into specialized cells destined to become leaves, stems or flowers.

The first identification of such a mechanism in plants is reported by Clark and his research associates in the
In addition to its significance for basic science, the discovery could have important applications in agriculture, according to Clark, an associate professor of biology at the U-M, who is affiliated with the U-M’s Center for Organogenesis. Clark says researchers could use genetic engineering technology to increase flower and fruit production, or to control the timing of fruit development.

Clark works with Arabidopsis, a plant often used to study plant genetics and development. In the Science paper, he explains how an Arabidopsis gene called CLAVATA3 encodes a small protein signal called a ligand, which hangs out near patches of unspecialized plant cells called meristems. Another gene, CLAVATA1, encodes a receptor molecule, which penetrates meristem cell walls, with half the receptor on the outside and half inside the cell membrane.

 Arabidopsis shoot meristems shown in these magnified images have started to grow and change. Eventually the tiny patch of undifferentiated cells in the inset image labeled “normal” will become the stems, leaves and flowers of a mature, living plant. The larger image labeled “mutant” shows a plant in which the CLAVATA3 gene is not working. Mutations in CLAVATA3 produce massive numbers of unspecialized cells—similar to a malignant tumor.

When the ligand binds to the outer half of the receptor, it triggers chemical changes inside the meristem cell. A series of messenger molecules carry these chemical signals to genes in the cell nucleus telling them to turn off the locking signal that keeps meristem cells from developing. Once the locking signal stops, the meristem begins forming a tiny plant shoot, which will grow into a stem and, eventually, leaves and flowers.

“We know of over 150 receptors similar to CLV1 in Arabidopsis, but little is known about how they function,” Clark says. “Similar structures also are involved in plant disease resistance and human hormone signaling. Understanding how CLV1 and CLV3 work will help scientists understand how the others work, as well.”

Like most scientific research, Clark says his discovery raises as many questions as it answers. One big mystery involves unusual two-way communication between the ligand and receptor. “The traditional view is that changes outside the cell membrane caused by ligand binding lead to changes inside the cell, which start the signaling process. For CLV1, it appears that information also flows from inside the cell to the outside. Unless it receives these chemical signals from inside the cell, the receptor will not bind to the ligand.”

Then there is the unknown role played by another gene, CLAVATA2. “All we know at the moment is that in plants, CLV2 is required to stabilize CLV1 protein,” Clark explains. “Without CLV2, CLV1 protein degrades.”

The U-M study was funded by the National Science Foundation‘s Developmental Mechanisms Program. Amy Trotochaud, U-M research associate, and Sangho Jeong, U-M graduate student, collaborated in the study.

The California Institute of Technology holds a patent for the use of CLAVATA1 in transgenic plants.

ImageSteven ClarkBiologyNational Science Foundation