Researchers at the Salk Institute for Biological Studies studying the frumpy wild mustard plant Arabidopsis thaliana rather than the elegant rose recently determined why plants with a defective TOPLESS gene form an extra root where the shoot should be. Their findings, published in the June 9th issue of the journal Science, suggest that it is possible to engineer a plant cell to develop in ways that better suit agricultural needs.
"If we know how a plant forms a root instead of a shoot, and that there is time in which to make such an important change, it might be possible to tell a plant to make a leaf instead of a flower," says the study's lead author, Jeffrey A. Long, Ph.D., an assistant professor in the Plant Molecular and Cellular Biology Laboratory. "We can now think about plant development in a different way."
The study, which included researchers from the laboratory of Elliot M. Meyerowitz, Ph.D., at the California Institute of Technology, specifically focused on understanding mutations in the TOPLESS gene that Long had previously identified in Arabidopsis thaliana, the first flowering plant to have its genome sequenced and a popular model organism for many aspects of plant biology.
Like animals, plants develop along a polar axis, but with a root on one end and a shoot on the other. A defective TOPLESS gene, however, causes plant embryos to develop into a seedling with two oppositely oriented root poles – hence the gene's name. Long asked how mutations in TOPLESS can switch a plant cell's fate from shoot to root, hoping to discover how cells at the "basal" end of plant embryos become roots, while cells at the top or "apical" end become shoots that give rise to leaves, branches, and flowers. "We want to know how a plant can set aside a root and a shoot pole during embryogenesis and keep these functions separate," Long says.
The researchers found that the TOPLESS gene encodes a protein (TOPLESS) that is a transcriptional co-repressor. In plants and animals, co-repressors regulate gene expression by inhibiting the activity of transcription factors, which act as switches to activate target genes. Transcription factors control gene activity by binding to DNA sequences adjacent to a gene, but they are deactivated when they recruit and interact with co-repressors.
Long explains that the normal function of TOPLESS protein is to silence genes required for root development in the top or shoot half of a plant embryo. "In plants with a mutant TOPLESS, genes that should be kept off in order to produce a shoot aren't, so a root is produced," he explains.
Since transcriptional repression plays such a key role in animal embryonic development, the finding that a co-repressor controls polarity in plants was surprising, says Long. "We thought that because plants and animals are believed to have largely developed independently from each other, they would have used a different set of processes to maintain polarity," he says. "But they have a very similar toolbox of genes to set up some aspects of their body plan."
However, a critical difference between plants and animals in terms of polarity development is how much more tolerant plants are of manipulation. Long says, "In animals, early cell divisions are very important to development of polarity and if something goes awry with co-repressors, the animal quickly dies. But in plants, polarity can be changed much later in embryogenesis."
"Plants are so plastic. Our topless mutants can survive very well," he continues. "This suggests that the actual polarity in the embryo isn't fixed until late in development, and that offers us an opportunity to change the fate of the plant structure."
Also contributing to this work were graduate student Zachery R. Smith at the Salk Institute and Carolyn Ohno, Ph.D., at the California Institute of Technology.
The Salk Institute for Biological Studies in La Jolla, California, is an independent nonprofit organization dedicated to fundamental discoveries in the life sciences, the improvement of human health and the training of future generations of researchers. Jonas Salk, M.D., whose polio vaccine all but eradicated the crippling disease poliomyelitis in 1955, opened the Institute in 1965 with a gift of land from the City of San Diego and the financial support of the March of Dimes.
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