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First published online December 16, 2005; 10.1104/pp.105.068874

Plant Physiology 140:235-248 (2006)
© 2006 American Society of Plant Biologists

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PLANTS INTERACTING WITH OTHER ORGANISMS

A Circadian Rhythm-Regulated Tomato Gene Is Induced by Arachidonic Acid and Phythophthora infestans Infection1,[W]

Philip D. Weyman, Zhiqiang Pan2, Qin Feng, David G. Gilchrist and Richard M. Bostock*

Department of Plant Pathology (P.D.W., Q.F., D.G.G., R.M.B.) and Center for Engineering Plants for Resistance Against Pathogens (Z.P., D.G.G., R.M.B.), University of California, Davis, California 95616

A cDNA clone of unknown function, DEA1, was isolated from arachidonic acid-treated tomato (Solanum lycopersicum) leaves by differential display PCR. The gene, DEA1, is expressed in response to the programmed cell death-inducing arachidonic acid within 8 h following treatment of a tomato leaflet, 16 h prior to the development of visible cell death. DEA1 transcript levels were also affected by the late blight pathogen, Phytophthora infestans. To gain further insight into the transcriptional regulation of DEA1, the promoter region was cloned by inverse PCR and was found to contain putative stress-, signaling-, and circadian-response elements. DEA1 is highly expressed in roots, stems, and leaves, but not in flowers. Leaf expression of DEA1 is regulated by circadian rhythms during long days with the peak occurring at midday and the low point midway through the dark period. During short days, the rhythm is lost and DEA1 expression becomes constitutive. The predicted DEA1 protein has a conserved domain shared by the eight-cysteine motif superfamily of protease inhibitors, {alpha}-amylase inhibitors, seed storage proteins, and lipid transfer proteins. A DEA1-green fluorescent protein fusion protein localized to the plasma membrane in protoplasts and plasmolysis experiments, suggesting that the native protein is associated with the plasmalemma in intact cells.


1 This work was supported by the U.S. Department of Agriculture-National Research Initiative program (grant no. 96–35303–3238) and the National Science Foundation Cooperative Agreement (grant no. BIR–8920216 to the Center for Engineering Plants for Resistance Against Pathogens).

2 Present address: U.S. Department of Agriculture, Agricultural Research Service, Natural Products Utilization Research Unit, University of Mississippi, P.O. Box 8048, University, MS 38677.

The author responsible for distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instructions for Authors (www.plantphysiol.org) is: Richard M. Bostock (rmbostock{at}ucdavis.edu).

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

Article, publication date, and citation information can be found at www.plantphysiol.org/cgi/doi/10.1104/pp.105.068874.

* Corresponding author; rmbostock{at}ucdavis.edu; fax 530–752–5674.

Received August 23, 2005; returned for revision November 3, 2005; accepted November 9, 2005.




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