To determine its function, they examined mutant plants harboring a disrupted AtABCG14 gene. They found that knocking out this transporter gene resulted in plants with weaker growth, slenderer stems, and shorter primary roots than their wild-type counterparts. These structural changes in the plants are symptoms of cytokinin deficiencies. Essentially, the long-distance transportation of the growth hormones is impaired, which causes alterations in the development of roots and shoots. The disrupted transport also resulted in losses of chlorophyll, the molecule that transforms absorbed sunlight into energy.
The team then used radiotracers to confirm the role of the AtABCG14 protein in transporting cytokinins through the plants. They fed Carbon-14-labeled cytokinins to the roots of both the wild-type and mutant seedlings. While the shoots of the wild-type plants were full of the hormones, there were only trace amounts in the shoots of the mutant plants, though their roots were enriched. This demonstrates a direct correlation between cytokinin transport and the action of AtABCG14 protein.
"Understanding the molecular basis for cytokinin transport enables us to more deeply appreciate how plants employ and distribute a set of signaling molecules to organize their life activity and for their entire body building," Liu said.
"From a biotechnology view, manipulating the activity of this identified transporter might afford us the flexibility to enhance the capacity and efficiency of plants in energy capture and transformation, and the storage of the reduced carbon, or the ability of plants to adapt to harsh environments, therefore promoting either the production of renewable feedstocks for fuels and bio-based materials, or grain yields to meet our world-wide food and energy demands."
|Contact: Chelsea Whyte|
DOE/Brookhaven National Laboratory