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First published online August 4, 2006; 10.1104/pp.106.085647

Plant Physiology 142:750-761 (2006)
© 2006 American Society of Plant Biologists

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ENVIRONMENTAL STRESS AND ADAPTATION TO STRESS

Quantitative Profiling of Arabidopsis Polar Glycerolipids in Response to Phosphorus Starvation. Roles of Phospholipases D{zeta}1 and D{zeta}2 in Phosphatidylcholine Hydrolysis and Digalactosyldiacylglycerol Accumulation in Phosphorus-Starved Plants1,[W]

Maoyin Li, Ruth Welti and Xuemin Wang*

Department of Biology, University of Missouri, St. Louis, Missouri 63121 (M.L., X.W.); Danforth Plant Science Center, St. Louis, Missouri 63132 (M.L., X.W.); and Division of Biology, Kansas State University, Manhattan, Kansas 66506 (R.W.)

Phosphorus is an essential macronutrient that often limits plant growth and development. Under phosphorus-limited conditions, plants undergo substantial alterations in membrane lipid composition to cope with phosphorus deficiency. To characterize the changes in lipid species and to identify enzymes involved in plant response to phosphorus starvation, 140 molecular species of polar glycerolipids were quantitatively profiled in rosettes and roots of wild-type Arabidopsis (Arabidopsis thaliana) and phospholipase D knockout mutants pld{zeta}1, pld{zeta}2, and pld{zeta}1pld{zeta}2. In response to phosphorus starvation, the concentration of phospholipids was decreased and that of galactolipids was increased. Phospholipid lost in phosphorus-starved Arabidopsis rosettes was replaced by an equal amount of galactolipid. The concentration of phospholipid lost in roots was much greater than in rosettes. Disruption of both PLD{zeta}1 and PLD{zeta}2 function resulted in a smaller decrease in phosphatidylcholine and a smaller increase in digalactosyldiacylglycerol in phosphorus-starved roots. The results suggest that hydrolysis of phosphatidylcholine by PLD{zeta}s during phosphorus starvation contributes to the supply of inorganic phosphorus for cell metabolism and diacylglycerol moieties for galactolipid synthesis.

1 This work was supported by the National Science Foundation (NSF; grant nos. MCB–0455318 and IOB–0454866) and by the U.S. Department of Agriculture (grant no. 2005–35818–15253). The Kansas Lipidomics Research Center Analytical Laboratory was supported by the NSF EPSCoR program (grant no. EPS–0236913) with matching support from the State of Kansas through the Kansas Technology Enterprise Corporation and Kansas State University. The Kansas Lipidomics Research Center also received Core Facility support from the K-IDeA Networks of Biomedical Research Excellence (INBRE) through the National Institutes of Health (grant no. P20RR16475 from the INBRE program of the National Center for Research Resources). This is contribution 06–323–J from the Kansas Agricultural Experiment Station.

The author responsible for distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instruction for Authors (www.plantphysiol.org) is: Xuemin Wang (wangxue{at}umsl.edu).

[W] The online version of this article contains Web-only data.

www.plantphysiol.org/cgi/doi/10.1104/pp.106.085647

* Corresponding author; e-mail wangxue{at}umsl.edu; fax 314–587–1519.

Received June 22, 2006; accepted July 28, 2006; published August 4, 2006.




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