CEPCEB Members

Elizabeth A. Bray Associate Professor Department of Botany and Plant Sciences University of California Riverside, CA 92521 Phone: (951) 827-4548 Fax: (951) 827-4437
Background Plant Water-Deficit Stress List of Relevant Publications (Bibliography page)

Background

I am interested in mechanisms that control tolerance of plants to water-deficit stress. This entails understanding the regulatory mechanisms that induce changes in gene expression and the function of the genes that are induced. The role of ABA in these responses is central to my research objectives.

I received my M.S. in Plant Physiology in 1978 and my Ph.D. from the University of Minnesota, St. Paul in 1982. This is where I became interested in the role that ABA plays in the plant stress response, and developed analytical tools to study plant hormones. I completed two postdoctoral studies. First, I studied ABA compartmentation at Michigan State University with Dr. Jan Zeevaart. Then I moved to Dr. Roger Beachy's lab at Washington University in St. Louis where I initiated my studies in the molecular role of ABA in seed biology.

Since joining the University of California Riverside in 1985, I have strengthened my interest in the mechanisms that control gene expression and the function of specific genes during stress. The group at UC Riverside fosters many tight interactions and collaborations. I have had joint projects with Patty Springer, Julia Bailey-Serres and Linda Walling.

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Plant Water-Deficit Stress

The proper amount of water is essential to plant growth and thus to plant production. When water is limiting a water-deficit stress is imposed on the plant, which limits crop production depending upon the severity, duration and rate of development of the stress. Therefore, it is important to understand the basic plant response to water-deficit stress in order to develop methods or management practices to improve crops for reduced water consumption. As a molecular biologist and plant physiologist, my contribution to this problem is to better understand the basic response of plants to water-deficit stress. As we develop a deeper understanding of the adaptive mechanisms and the injuries that occur in response to limited water, we will be able to improve our crops for production in unfavorable environments.

In order to fully understand the plant response to water deficit, we must be able to globally characterize changes in gene expression. This involves answering three main questions: (1) What are the changes in gene expression that occur in response to water deficit?; (2) How are the changes in gene expression regulated?; and (3) What are the functions of the gene products that are increased or decreased? Although these questions have been addressed for more than 15 years, we still have only rudimentary answers. New developments in plant genomics research and techniques will further our ability to answer these questions.

Signaling in the cell subjected to water-deficit stress is beginning to be unraveled (Fig. 1). We are interested in the mechanisms that control ABA biosynthesis and the subsequent signal transduction pathways. We are also initiating studies on the interactions of ABA with other plant hormones and other potential signaling molecules in the plant stress response.

Two genetic methods are being used to determine the function of specific genes in response to water-deficit stress. First, single gene mutants, disrupted in functions that are required for gene regulation in response to water-deficit stress, are being identified. The promoter from an ABA- and water-deficit-induced gene of tomato, le25, has been fused with adh and placed in an Arabidopsis genotype that is adh null. Seeds of a homozygous line containing this construct were treated with EMS, and pools of seeds were collected from the mutagenized parents. The seed pools were grown on agar plates in high humidity. When seedlings were 7 days old, they were moved to plates conditioned with PEG at a low water potential, and thus the seedlings were subjected to water-deficit stress. After a 2-hr allyl alcohol treatment, which causes a toxic substance (acrolein) to be synthesized in the presence of ADH activity, the seedlings were placed back in non-stress conditions. Seedlings unable to induce the le25 promoter will not have ADH activity and thus will survive. Seedlings in which the le25 promoter is induced will have sufficient ADH activity and will be killed by acrolein. Putative mutants have been selected by this method and are currently being characterized.

In a second method, enhancer/gene trap lines raised at UCR in collaboration with Patty Springer, are being screened for patterns in expression of the reporter gene that are altered by water-deficit stress. Reporter gene patterns have been found that are up-regulated and down-regulated by water-deficit stress. Fig. 2 illustrates an example of reporter gene expression that is up-regulated. In this line (GTR278), the gene trap landed in a gene encoding a receptor-like kinase (RLK). We are continuing to characterize this gene and identifying knock-outs in another RLK gene that is closely related to GTR278.

Selected Publications (Bibliography page)

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