2008年1月24日，北京生命科学研究所邓兴旺实验室在Nature杂志上发表题为 “Coordinated regulation of Arabidopsis thaliana development by light and gibberellins” 的文章。
该文报道了GA信号和光信号转导途径之间的相互作用分子机理。在GA不存在的条件下，核内定位的GA下游的转录因子DELLA蛋白积累到较高的水平，与光敏色素作用因子PIF3（bHLH类转录因子）结合，抑制PIF3结合其靶基因的启动子并调节基因表达，从而PIF3介导的光控的下胚轴伸长也受到抑制。而在GA存在的条件下，GA的受体GID1在核内与DELLA蛋白的结合能力提高，引发DELLA蛋白的泛素化并通过蛋白降解途径降解，释放与DELLA蛋白结合的PIF3蛋白，让它能够调节下游靶基因的表达，影响植物发育。
该项工作由美国耶鲁大学和北京生命科学研究所的邓兴旺实验室联合完成，该工作的第一作者冯夙化（已毕业耶鲁大学博士生）在耶鲁大学和北京生命科学研究所的邓兴旺实验室进行了该项目的研究，我所的周君莉博士、王峰（在读博士生）、陈力颖和禹露同学参与了此项工作。其它合作单位包括中科院遗传所和北京大学生科院。（生物谷Bioon.com）
生物谷推荐原始出处：
Nature 451, 475-479 (24 January 2008) | doi:10.1038/nature06448
Coordinated regulation of Arabidopsisthaliana development by light and gibberellins
Suhua Feng1,2,7, Cristina Martinez1,8, Giuliana Gusmaroli1,8, Yu Wang3,8, Junli Zhou2,8, Feng Wang2, Liying Chen2, Lu Yu2, Juan M. Iglesias-Pedraz4, Stefan Kircher5, Eberhard Sch?fer5, Xiangdong Fu6, Liu-Min Fan3 & Xing Wang Deng1,2,3
1 Department of Molecular, Cellular and Developmental Biology, Yale University, New Haven, Connecticut 06520-8104, USA
2 National Institute of Biological Sciences, Zhongguancun Life Science Park, Beijing 102206, China
3 Peking–Yale Joint Center for Plant Molecular Genetics and Agrobiotechnology, and National Laboratory for Protein Engineering and 4 Plant Genetic Engineering, College of Life Sciences, Peking University, Beijing 100871, China
5 Departamento Genética Molecular de Plantas, Centro Nacional de Biotecnología-CSIC, Campus Universidad Autónoma de Madrid, 28049 Madrid, Spain
6 Institut für Biologie II/Botanik, Albert Ludwigs Universit?t, Freiburg D-79104, Germany
7 Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100080, China
8 Present address: Howard Hughes Medical Institute, University of California at Los Angeles, Los Angeles, California 90095-1606, USA.
9 These authors contributed equally to this work.
Light and gibberellins (GAs) mediate many essential and partially overlapping plant developmental processes. DELLA proteins are GA-signalling repressors that block GA-induced development1. GA induces degradation of DELLA proteins via the ubiquitin/proteasome pathway2, but light promotes accumulation of DELLA proteins by reducing GA levels3. It was proposed that DELLA proteins restrain plant growth largely through their effect on gene expression4, 5. However, the precise mechanism of their function in coordinating GA signalling and gene expression remains unknown. Here we characterize a nuclear protein interaction cascade mediating transduction of GA signals to the activity regulation of a light-responsive transcription factor. In the absence of GA, nuclear-localized DELLA proteins accumulate to higher levels, interact with phytochrome-interacting factor 3 (PIF3, a bHLH-type transcription factor) and prevent PIF3 from binding to its target gene promoters and regulating gene expression, and therefore abrogate PIF3-mediated light control of hypocotyl elongation. In the presence of GA, GID1 proteins (GA receptors) elevate their direct interaction with DELLA proteins in the nucleus, trigger DELLA protein's ubiquitination and proteasome-mediated degradation, and thus release PIF3 from the negative effect of DELLA proteins.
