Plant and Cell Physiology Advance Access originally published online on March 7, 2005
Plant and Cell Physiology 2005 46(4):547-556; doi:10.1093/pcp/pci072
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ACTIVATOR of Spomin::LUC1/WRINKLED1 of Arabidopsis thaliana Transactivates Sugar-inducible Promoters
1 Laboratory of Biochemistry, Graduate School of Bioagricultural Science, Nagoya University, Chikusa, Nagoya, 464-8601 Japan
2 Faculty of Agriculture, Meijo University, Tenpaku, Nagoya, 468-8502 Japan
4 Corresponding author: E-mail, kenzo{at}agr.nagoya-u.ac.jp; Fax, +81-52-789-4094.
We isolated an enhancer activation-tagged mutant of Arabidopsis thaliana line sGsL carrying the luciferase (LUC) gene under control of a short sugar-inducible promoter derived from a sweet potato sporamin gene (Spo min) that showed high level expression of LUC under non-inducing conditions. The activator of Spo min ::LUC1 (ASML1) gene located downstream of the enhancer encoded an APETALA2 (AP2)-type AP2 domain protein, and this gene was shown recently to be responsible for the wrinkled1 mutation which causes defective accumulation of seed storage oil. Overexpression of ASML1 cDNA in sGsL plants resulted in enhanced expression of not only the LUC reporter but also endogenous sugar-inducible genes including Atß-Amy encoding ß-amylase. Transient co-expression of 35S::ASML1 with Spo min ::LUC or Atß-Amy::LUC reporters in protoplasts resulted in an approximately 10-fold transactivation of LUC expression. This transactivation was lost when the C-terminal acidic region of ASML1 was deleted. Expression of ASML1 was high in reproductive organs, and ASML1 mRNA showed transient accumulation in leaves after treatment with 6% sucrose, whereas it did not respond to abscisic acid. These results suggest that ASML1/WRI1 is a transcriptional activator involved in the activation of a subset of sugar-responsive genes and the control of carbon flow from sucrose import to oil accumulation in developing seeds.
3 Present address: Nagoya University of Arts and Sciences, Nissin, Aichi, 470-0196 Japan.
Received January 26, 2005; Accepted February 14, 2005
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