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Title: PHOSPHORUS DEFICIENCY IN WHITE LUPIN ALTERS ROOT DEVELOPMENT AND METABOLISM

Author
item GILBERT, GLENA - UNIVERSITY OF MINNESOTA
item ALLAN, DEBORAH - UNIVERSITY OF MINNESOTA
item Vance, Carroll

Submitted to: Annual Penn State Symposium in Plant Physiology
Publication Type: Proceedings
Publication Acceptance Date: 7/28/1997
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Phosphorus (P), an essential nutrient for plants, is limiting in many arable soils. White lupin has evolved several mechanisms for scavenging phosphate. We have characterized responses in lupin roots that occur during P deficient conditions. Proteoid root segments are visible by 9 days after emergence, and within 24 hours, higher phosphoenolpyruvate carboxylase (PEPC) mRNA levels are observed in the proteoid segments. In the following 48 hours, higher PEPC and APase activities are observed, and enhanced organic acid exudation is detected. Further work studying the regulation of PEPC and APase expression and the role of plant growth regulators in proteoid root formation will provide insight into the adaptive mechanisms used by white lupin to overcome P deficiency. Phosphate regulated gene expression has been well characterized in bacteria and fungi. In Escherichia coli, an element that regulates up to 20 genes, pho B, is induced during P deficient conditions. The Pi status in E. coli has been found to regulate up to 3% of the entire genome. Characterization of coordinated responses to P stress in many plants suggests that higher plants may also contain P driven regulatory mechanisms, although a comparable pho regulon has not been found in higher plants. Further studies of the biochemical and molecular responses of higher plants are needed to define features controlling plant responses to nutritional deficiencies and confirm the existence of a pho like region. The coordinated anatomical and biochemical changes that occur in white lupin roots make it a useful model for studying the responses of higher plants to P deficiency.