Studies on the regulation of elongation growth by gibberellins

赤霉素（giberellins, GAs）是植物发育许多方面的重要调控因子，包括种子萌发、茎伸长、花诱导和花药发育。内源性发育程序和环境刺激都会影响这些酶的表达。因此，阐明GA生物合成酶的转录调控对于确定参与植物发育的分子机制以及了解这些机制如何帮助植物适应环境变化至关重要。RSG是一种烟草（Nicotiana tabacum）转录激活因子，具有基本的亮氨酸拉链结构域，通过控制GA生物合成酶来调节内源性GAs的量。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易位进入细胞核是对GA水平降低的反应。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。相比之下，不能与14-3-3结合的突变体RSG （S114A）在GA作用后仍主要定位于细胞核内。对GA生物合成基因mRNA水平的分析表明，在表达RSG显性阴性形式的转基因植株中，GA 20氧化酶基因的反馈调控被抑制。我们的研究结果表明，RSG通过14-3-3结合被GA负向调节，并可能参与GA的内稳态。

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.