2005 Fiscal Year Final Research Report Summary
Studies on the regulation of elongation growth by gibberellins
Project/Area Number |
14340249
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
植物生理
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Research Institution | HIR0SHIMA UNIVERSITY |
Principal Investigator |
TAKAHASHI Yohsuke Hiroshima University, Graduate School of Science, Profeesor, 大学院・理学研究科, 教授 (90183855)
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Project Period (FY) |
2002 – 2005
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Keywords | Gibberellin / Transcription factor / 14-3-3 / Intracellular localization / CDPK / Phosphorylation |
Research Abstract |
Gibberellins (GAs) are essential regulators of many aspects of plant development, including seed germination, stem elongation, flower induction, and anther development. Both endogenous developmental programs and environmental stimuli affect the expression of these enzymes. Therefore, elucidating the transcriptional regulation of GA biosynthetic enzymes is crucial to identify the molecular mechanisms involved in plant development and to understand how these mechanisms help plants adapt to changes in their environment. RSG is a tobacco (Nicotiana tabacum) transcriptional activator with a basic Leu zipper domain that regulates endogenous amounts of GAs by the control of a GA biosynthetic enzyme. The 14-3-3 signaling proteins have been suggested to suppress RSG by sequestering it in the cytoplasm. We found that GA levels regulate the intracellular localization of RSG. RSG translocated into the nucleus in response to a reduction in GA levels. GA treatment could reverse this nuclear accumulation. The GA-induced disappearance of RSG-green fluorescent protein from the nucleus did not depend on protein degradation. By contrast, the mutant RSG (S114A) that could not bind to 14-3-3 continued to be localized predominantly in the nucleus after GA application. Analysis of the mRNA levels of GA biosynthetic genes showed that the feedback regulation of the GA 20-oxidase gene was inhibited in transgenic plants expressing a dominant negative form of RSG. Our results suggest that RSG is negatively modulated by GAs by 14-3-3 binding and might be involved in GA homeostasis.
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Research Products
(10 results)