Studies on the regulation of elongation growth by gibberellins

赤霉素（GAs）是植物生长发育的重要调节因子，在种子萌发、茎伸长、花诱导和花药发育等过程中起着重要作用。内源性发育程序和环境刺激都影响这些酶的表达。因此，阐明GA生物合成酶的转录调控是至关重要的，以确定参与植物发育的分子机制，并了解这些机制如何帮助植物适应环境的变化。RSG是烟草（Nicotiana tabacum）的转录激活因子，其具有通过控制GA生物合成酶来调节内源性GA量的碱性Leu拉链结构域。14-3-3信号蛋白被认为通过将RSG隔离在细胞质中来抑制RSG。我们发现GA水平调节RSG的细胞内定位。RSG易位到细胞核中，以响应GA水平的降低。GA处理可以逆转这种核积累。GA诱导的RSG-绿色荧光蛋白从细胞核中消失不依赖于蛋白质降解。相反，不能与14-3-3结合的突变体RSG（S114 A）在GA应用后继续主要定位在细胞核中。GA生物合成基因的mRNA水平的分析表明，反馈调节的GA 20-氧化酶基因被抑制在转基因植物表达显性负形式的RSG。我们的研究结果表明，RSG是负调节GA通过14-3-3结合，并可能参与GA的稳态。

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.