한빛사논문
Abstract
Young-Hee Cho, Sang-Dong Yoo*
Department of Biological Science, Sungkyunkwan University, Suwon, Korea
Abstract
Sugars are evolutionarily conserved signaling molecules that regulate the growth and development of both unicellular and multicellular organisms. As sugar-producing photosynthetic organisms, plants utilize glucose as one of their major signaling molecules. However, the details of other sugar signaling molecules and their regulatory factors have remained elusive, due to the complexity of the metabolite and hormone interactions that control physiological and developmental programs in plants. We combined information from a gain-of-function cell-based screen and a loss-of-function reverse-genetic analysis to demonstrate that fructose acts as a signaling molecule in Arabidopsis thaliana. Fructose signaling induced seedling developmental arrest and nteracted with plant stress hormone signaling in a manner similar to that of glucose. For fructose signaling responses, the plant glucose sensor HEXOKINASE1 HXK1) was dispensable, while FRUCTOSE INSENSITIVE1 (FINS1), a putative FRUCTOSE-1,6-BISPHOSPHATASE, played a crucial role. Interestingly, FINS1 function in fructose signaling appeared to be independent of its catalytic activity in sugar metabolism. Genetic analysis further indicated that FINS1. dependent fructose signaling may act downstream of the abscisic acid pathway, in spite of the fact that HXK1.dependent glucose signaling works upstream of hormone synthesis. Our findings revealed that multiple layers of controls by fructose, glucose, and abscisic acid finely tune the plant autotrophic transition and modulate early seedling establishment after seed germination.
Citation: Cho Y-H, Yoo S-D (2011) Signaling Role of Fructose Mediated by FINS1/FBP in Arabidopsis thaliana. PLoS Genet 7(1): e1001263. doi:10.1371/ journal.pgen.1001263
Editor: Gregory P. Copenhaver, The University of North Carolina at Chapel Hill, United States of America
Received April 30, 2010; Accepted November 30, 2010; Published January 6, 2011
Copyright: 2011 Cho, Yoo. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: This work was supported by Korean National Research Foundation to S-DY (2010-0015456, 2010-0016509) and Y-HC (2010-0007068). The funder had no rule in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing Interests: The authors have declared that no competing interests exist.
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