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Title: SIGNALING OF PHOSPHORUS DEFICIENCY INDUCED GENE EXPRESSION IN WHITE LUPIN REQUIRES SUGARS AND PHLOEM TRANSPORT

Author
item LIU, JUNQI - UNIVERSITY OF MINNESOTA
item Samac, Deborah - Debby
item Bucciarelli, Bruna
item ALLAN, DEBORAH - UNIVERSITY OF MINNESOTA
item Vance, Carroll

Submitted to: Plant Journal
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/22/2004
Publication Date: 1/1/2005
Citation: Liu, J., Samac, D.A., Bucciarelli, B., Allan, D.L., Vance, C.P. 2005. Signaling of phosphorus deficiency induced gene expression in white lupin requires sugars and phloem transport. Plant Journal. 41:257-268.

Interpretive Summary: Management of the soil nutrient phosphorus (P) in agriculture poses a conundrum. Although P is required for plant growth, most agricultural soils are deficient in this nutrient. In developed countries, P-deficient soils are remedied by adding P fertilizer. However, because plants are inefficient at obtaining the added P, fields are heavily fertilized to ensure crops receive a sufficient supply. This results in overloading of fields with P and subsequent pollution of water supplies. By contrast, lack of available P fertilizer in developing countries limits crop production. If plants could be made more efficient in obtaining P from soil, the P conundrum could be alleviated. The objectives of this study were to determine if there are common elements controlling plant genes involved in P utilization and what plant components are important in regulating the activity of genes involved in P use. The results show that DNA sequences within the region controlling genes involved in P utilization in lupin plants are very similar to those in alfalfa and Arabidopsis. In fact, these DNA sequences are interchangeable between plants. In addition, sugars derived from photosynthesis play a major role in turning P use genes off and on. This work is important because it: 1) identifies new genetic elements controlling P utilization genes; and 2) shows that P nutrient stress is cross linked with photosynthesis and sugars. This information will be useful in designing plants that can more efficiently take up and utilize P. Success in developing plants that are more efficient in P nutrition will help reduce overuse of P fertilizer.

Technical Abstract: Roots of phosphorus (P) deficient white lupin exhibit striking changes in morphology and gene expression. In this report we provide further insight into genetic elements affecting transcription of P-deficiency induced genes. Moreover, we also show that sugars and photosynthate are integrally related to P-deficiency induced gene expression. White lupin phosphate transporter (LaPT1) and secreted acid phosphatase (LaSAP1) promoter-reporter genes when transformed into alfalfa, a heterologous legume, showed significant induction in roots specifically in response to P-deficiency. In addition, both promoters were active in nitrogen-fixing root nodules but not in ineffective nodules indicating a link between P-deficiency and factors related to nitrogen fixation/metabolism. Because sugars are known to play a role in signal transduction during nitrogen assimilation and are required for effective nitrogen fixation, we tested the relationship of sugars to P-deficiency induced gene expression. Exogenous sucrose, glucose, and fructose stimulated LaPT1 and LaSAP1 transcript accumulation in dark-grown P-sufficient white lupin seedlings. Furthermore, in intact P-deficient white lupin plants, LaPT1 and LaSAP1 expression in cluster roots was strikingly reduced in dark-adapted plants with expression rapidly restored upon re-exposure to light. Likewise, interruption of phloem supply to P-deficient roots resulted in a rapid decline in LaPT1 and LaSAP1 transcript accumulation. Similar results were also obtained with a third lupin P-deficiency induced gene encoding a putative multidrug and toxin efflux protein (LaMATE). Inclusively our data show that the regulation of P-deficiency induced genes is conserved across plant species and sugars/photosynthate are crucial for P-deficiency signal transduction.