Analysis of a Light-Regulated Development Switch

光控开发开关的分析

• 批准号: 6837076
• 负责人: XING WANG DENG
• 金额: $ 55.88万
• 依托单位: YALE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 1992
• 资助国家: 美国
• 起止时间: 1992-08-01 至 2009-01-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6837076
• 关键词: Arabidopsis; biological signal transduction; developmental genetics; gene expression; gene mutation; genetic regulatory element; genome; molecular cloning; nonvisual photoreceptor; photobiology; plant genetics; plant growth /development; plant proteins; protein protein interaction; protein structure function; transcription factor

DESCRIPTION (provided by applicant): Light signals from the environment are perceived by distinct classes of photoreceptors and transduced to the nuclear regulators to control the developmental modes, largely through regulated gene expression. The long-term goal of our research is to dissect the cellular and biochemical basis of this light control of development switch. Our previous work, together with studies from others, has defined a group of evolutionarily conserved COP/DET/FUS proteins that act as light inactivatable repressor of photomorphogenesis. We have established that Arabidopsis COP1 (constitutively photomorphogenic 1) acts within nucleus to suppress the photomorphogenic developmental pathway in darkness and light reverses this repressive action and deplete its nuclear accumulation. Our current NIH funded studies indicates that once within the nucleus, COP1, together with COP10 complex, the COP9 signalosome, and DET1 complex, physically contact and target specific transcription factors (including HY5 and HYH) for ubiquitination and proteasome mediated degradation. The activities of those transcription factors are responsible for promoting photomorphogenic development and gene expression. We also made important progresses in understanding how blue and far red light, once perceived by cryptochromes and phytochrome A, transduced to regulate this switch. Here I propose to combine molecular genetic, biochemical, proteomic, and genomic approaches to comprehensively analyze this regulatory network at the levels of biochemical composition and action, network interactions of the components, and their mediation of light control of genome expression and development. To achieve this goal, I propose three major complementary aspects of further research with eight specific Objectives. The first aspect, including Objectives I to III, is basically to confirm the hypothesized biochemical activities and to reveal the molecular constitutes of the two major players, the COP1 and COP10 complexes. The second aspect, including Objectives IV and VI, is to how far red and blue light signal regulate the COP1 switch through their own photoreceptors and signaling events. The third aspect, including Objectives VII to VIII, is to provide a whole genome level understanding on light control of gene expression and reveal the transcriptional cascade/network at a genomic scale. The accomplishment of these proposed objectives shall provide a comprehensive and mechanistic view of the signaling network responsible for light control of development. This should serve as an essential guidance for investigating similar issues in mammals including human.

描述（由申请人提供）：来自环境的光信号被不同类别的光感受器所感知，并将其传递到核调节剂中以控制发育模式，这在很大程度上通过调节的基因表达。我们研究的长期目标是剖析这种开发转换的光控制的细胞和生化基础。我们以前的工作以及来自其他研究的研究定义了一组进化保守的COP/DET/FUS蛋白质，这些蛋白充当光态生成的轻度不可分割的阻遏物。我们已经确定，拟南芥COP1（组成性的显微形态学1）在核中起作用，以抑制黑暗中的光性发育途径，而光逆转了这种抑制作用并耗尽了其核积累。我们当前的NIH资助研究表明，一旦在核，COP1内，COP10复合物，COP9信号体和DET1复合物，物理接触并靶向特定的转录因子（包括HY5和HYH），用于泛素化和蛋白酶体介导的降解。这些转录因子的活性负责促进光性发育和基因表达。我们还取得了重要的进步，以了解一旦被加密斑块和植物色素A感知的蓝色和遥远的红色光线如何转导用于调节此开关。在这里，我建议将分子遗传，生化，蛋白质组学和基因组方法结合在一起，以全面地分析生化组成和作用水平的该调节网络，成分的网络相互作用以及它们对基因组表达和发育的光控制的中介。为了实现这一目标，我提出了进一步研究的三个主要互补方面，并提出了八个特定目标。第一方面（包括目标I至III）基本上是确认假设的生化活动，并揭示两个主要参与者COP1和COP10复合物的分子构成。包括目标IV和VI在内的第二个方面是红色和蓝光信号通过其自己的光感受器和信号事件进行了多远调节COP1开关。第三个方面，包括目标VII到VIII，是为基因表达的光控制提供全基因组水平的理解，并以基因组规模揭示转录级联/网络。这些提议的目标的实现应提供负责开发光控制的信号网络的全面和机械观点。这应该是调查包括人类在内的哺乳动物类似问题的重要指导。