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

摘要 细胞器基因表达的控制对于所有真核生物的细胞编程是至关重要的。 虽然扰乱线粒体基因表达会导致人类病理学，包括癌症，但改变 质体基因表达可以杀死植物。然而，控制细胞器的细胞信号机制 基因表达仍然知之甚少。PI实验室的长期目标是利用 光受体调控拟南芥叶绿体生物发生作为理解细胞遗传模型 控制细胞器基因表达的信号机制。目前的数据支持中央 假设红色和远红色光感受器，光敏色素，诱导质体的表达- 编码光合作用相关基因，通过细胞核到质体的信号传导，激活细菌， 型质体RNA聚合酶。在这里，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，以（1）确定激活 质体中细菌型RNA聚合酶的作用机制，（2）鉴定核质信号， 触发质体RNA聚合酶的激活，以及（3）确定光敏色素信号传导 启动细胞核中的细胞核到质体信号传导的机制。拟议的研究是 创新，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一种 遗传模型来研究以前未表征的细胞核到细胞器信号通路。的PI 已经开发了新的正向遗传筛选和生物化学测定，以识别 核质信号转导，并阐明其信号转导机制。拟议的研究意义重大， 因为它有望揭示控制质体转录的光感受器信号机制- 这是我们对植物光信号和叶绿体生物发生认识的一个长期空白。因为 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， 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， 因此，最终将有助于理解错误监管的机制， 线粒体基因在人类疾病中的表达。

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.