Mechanism of nucleus-to-plastid light signaling in controlling plastid transcription

核到质体光信号传导控制质体转录的机制

• 批准号: 10375791
• 负责人: Meng Chen
• 金额: $ 5.71万
• 依托单位: UNIVERSITY OF CALIFORNIA RIVERSIDE
• 依托单位国家: 美国
• 财政年份: 2020
• 资助国家: 美国
• 起止时间: 2020-02-07 至 2023-12-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/10375791
• 关键词: Arabidopsis; Biochemical; Biochemistry; Biogenesis; Biological Assay; Cell Nucleus; Cellular biology; Chloroplasts; DNA-Directed RNA Polymerase; Data; Gene Expression; Genes; Genetic Models; Genetic Screening; Genetic Transcription; Genomic approach; Goals; Human; Human Pathology; Knowledge; Laboratories; Lead; Learning; Light; Malignant Neoplasms; Mission; Mitochondria; Modeling; Molecular Genetics; Organelles; Organism; Photoreceptors; Photosynthesis; Phytochrome; Plants; Plastids; Public Health; Regulation; Research; Signal Pathway; Signal Transduction; Transcriptional Regulation; United States National Institutes of Health; disability; human disease; innovation; structural biology

Abstract The control of organellar gene expression is critical for cellular programming of all eukaryotic organisms. While perturbing mitochondrial gene expression leads to human pathologies, including cancer, altering plastidial gene expression can kill plants. However, the cell signaling mechanisms that control organellar gene expression remain poorly understood. The long-term goal of the PI’s laboratory is to utilize photoreceptor-regulated chloroplast biogenesis in Arabidopsis as a genetic model to understand cell signaling mechanisms controlling organellar gene expression. The current data support the central hypothesis that the red and far-red photoreceptors, the phytochromes, induce the expression of plastid- encoded photosynthesis-associated genes through nucleus-to-plastid signaling that activates a bacterial- type plastidial RNA polymerase. Here the PI propose to utilize a combination of molecular genetics, biochemistry, structure biology, cell biology, and genomics approaches to (1) determine the activation mechanism of the bacterial-type RNA polymerase in plastids, (2) identify the nucleus-to-plastid signal that triggers the activation of the plastidial RNA polymerase, and (3) determine the phytochrome signaling mechanism that initiates the nucleus-to-plastid signaling in the nucleus. The proposed research is innovative because it utilizes photoreceptor signaling and chloroplast biogenesis in Arabidopsis as a genetic model to investigate a previously uncharacterized nucleus-to-organelle signaling pathway. The PI has developed new forward genetic screens and biochemical assays to identify components in the nucleus-to-plastid signaling and elucidate their signaling mechanisms. The proposed research is significant, because it is expected to uncover the photoreceptor signaling mechanisms controlling plastidial transcription - a long-standing gap in our knowledge of plant light signaling and chloroplast biogenesis. Because the control of transcription in plastids shares many similarities with that in mitochondria, what we learn in the plastid model is expected to enhance the understanding of the general principles of cell signaling mechanisms in controlling organellar gene expression, including the regulation of mitochondrial gene expression, and therefore, will ultimately contribute to the understanding of the mechanisms underlying the misregulations of mitochondrial gene expression in human diseases.

抽象的 细胞器基因表达的控制对于所有真核生物的细胞编程至关重要。 虽然扰乱线粒体基因表达会导致包括癌症在内的人类疾病，但 质体基因表达可以杀死植物，但是控制细胞器的细胞信号传导机制。 PI 实验室的长期目标是利用基因表达。 拟南芥中光感受器调节的叶绿体生物发生作为理解细胞的遗传模型 控制细胞器基因表达的信号机制。目前的数据支持中央。 假设红色和远红光感受器（光敏色素）诱导质体表达 通过核到质体信号传导编码光合作用相关基因，激活细菌- 在此，PI 建议利用分子遗传学的组合， 生物化学、结构生物学、细胞生物学和基因组学方法（1）确定激活 质体中细菌型 RNA 聚合酶的机制，(2) 识别核到质体的信号 触发质体 RNA 聚合酶的激活，并且 (3) 确定光敏色素信号传导 拟议的研究是在细胞核中启动细胞核到质体信号传导的机制。 创新性是因为它利用拟南芥中的光感受器信号传导和叶绿体生物发生作为 遗传模型来研究以前未表征的细胞核到细胞器信号通路。 开发了新的正向遗传筛选和生化检测来鉴定 核到质体信号传导并阐明其信号传导机制具有重要意义。 因为它有望揭示控制质体转录的光感受器信号传导机制 - 我们在植物光信号和叶绿体生物发生方面的知识长期存在差距。 质体中的转录控制与线粒体中的转录控制有许多相似之处，我们在 质体模型有望增强对细胞信号传导机制一般原理的理解 控制细胞器基因表达，包括线粒体基因表达的调节，以及 因此，最终将有助于理解错误监管的机制 人类疾病中的线粒体基因表达。