Coordinated regulation of Arabidopsis thaliana development by light and gibberellins

Coordinated regulation of Arabidopsis thaliana development by light and gibberellins
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光和赤霉素对拟南芥发育的协调调控

DOI:
10.1038/nature06448
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发表时间:
2008-01-24
期刊:
影响因子:
64.8
通讯作者:
Deng, Xing Wang
Deng, Xing Wang
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Feng, Suhua;Martinez, Cristina;Deng, Xing Wang

文献摘要

被引文献

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光和赤霉素(GAs)调节许多必要的和部分重叠的植物发育过程。Della蛋白是GA信号抑制因子,可以阻止GA诱导的发育。GA通过泛素/蛋白酶体途径诱导DELLA蛋白的降解,但光通过降低GA水平促进DELLA蛋白的积累。有人认为Della蛋白主要通过影响基因表达来抑制植物的生长。然而,它们在协调GA信号和基因表达方面的确切作用机制仍不清楚。在这里,我们描述了核蛋白相互作用的级联,介导GA信号到光响应转录因子的活性调节的转导。在没有GA的情况下,核定位的Della蛋白积累到较高水平,与光敏色素相互作用因子3(PIF3,一种bHLH型转录因子)相互作用,阻止PIF3与其靶基因启动子结合并调节基因表达,从而取消PIF3介导的光控制下胚轴伸长。在GA存在的情况下,GID1蛋白(GA受体)与细胞核中的Della蛋白直接相互作用,触发Della蛋白的泛素化和蛋白酶体介导的降解,从而释放PIF3,使其脱离Della蛋白的负向作用。
Light and gibberellins (GAs) mediate many essential and partially overlapping plant developmental processes. DELLA proteins are GA-signalling repressors that block GA-induced development. GA induces degradation of DELLA proteins via the ubiquitin/proteasome pathway, but light promotes accumulation of DELLA proteins by reducing GA levels. It was proposed that DELLA proteins restrain plant growth largely through their effect on gene expression. 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.