2008年1月24日,，北京生命科學(xué)研究所鄧興旺實驗室在Nature雜志上發(fā)表題為 “Coordinated regulation of Arabidopsis thaliana development by light and gibberellins” 的文章,。
該文報道了GA信號和光信號轉(zhuǎn)導(dǎo)途徑之間的相互作用分子機理。在GA不存在的條件下,，核內(nèi)定位的GA下游的轉(zhuǎn)錄因子DELLA蛋白積累到較高的水平,，與光敏色素作用因子PIF3（bHLH類轉(zhuǎn)錄因子）結(jié)合，抑制PIF3結(jié)合其靶基因的啟動子并調(diào)節(jié)基因表達,，從而PIF3介導(dǎo)的光控的下胚軸伸長也受到抑制,。而在GA存在的條件下，GA的受體GID1在核內(nèi)與DELLA蛋白的結(jié)合能力提高,，引發(fā)DELLA蛋白的泛素化并通過蛋白降解途徑降解,，釋放與DELLA蛋白結(jié)合的PIF3蛋白,，讓它能夠調(diào)節(jié)下游靶基因的表達，影響植物發(fā)育,。
該項工作由美國耶魯大學(xué)和北京生命科學(xué)研究所的鄧興旺實驗室聯(lián)合完成,，該工作的第一作者馮夙化（已畢業(yè)耶魯大學(xué)博士生）在耶魯大學(xué)和北京生命科學(xué)研究所的鄧興旺實驗室進行了該項目的研究，我所的周君莉博士,、王峰（在讀博士生）,、陳力穎和禹露同學(xué)參與了此項工作。其它合作單位包括中科院遺傳所和北京大學(xué)生科院,。（生物谷Bioon.com）
生物谷推薦原始出處：
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.
