COPPER-RESPONSIVE SIGNAL TRANSDUCTION

描述：当莱茵衣原体面临铜缺乏时， 改变了主要代谢途径光合作用的组成， 用血红素蛋白质细胞色素c6取代铜蛋白质质体蓝素。 Cyt C6是由Cyc6基因的转录激活产生的， 相关的铜反应元件，而质体蓝素的损失是由调节 脱辅基蛋白的蛋白水解。其他适应性过程 包括Cpxl的转录激活，编码 粪卟啉原氧化酶-一种血红素生物合成酶，和Crdl，一种新的 二铁酶，假设其参与质体铁 动员，也许作为一个备份版本的plastidlocalized，多铜 氧化酶。涉及还原酶和转运蛋白的铜摄取途径， 也诱导。CRR1基因座的突变定义了一个主调节因子， 铜响应信号转导。这种调节分子似乎是 也参与了生物体对缺氧的反应， Cu（II）基氧化还原传感器。该系统提供了一个独特的机会， 了解和发现铜稳态过程中发生的细胞过程 in the context背景of deficiency缺陷.在人类中，铜缺乏症可能是由于 营养，特别是在婴儿，或从铜遗传疾病 代谢，如Menkes病。本研究的目的是：（1） 推断Crdl（推定的二铁酶）及其同系物Cthl的功能， 通过测定它们催化的反应，它们的亚细胞器 表达的位置和模式，评估Crdl是否是 铜酶，crdl突变株的表型分析，及其 与缺铁细胞的比较; 2）了解 目的：探讨铜蓝蛋白的操作及应用 呼吸作用中的铜酶与光合作用和铁代谢 适应C。reinhardtii铜缺乏症，并发现新的 铜响应靶点和铜代谢蛋白;以及3）鉴定 一个关键的调节器，Crrl，在铜响应信号转导途径， 互补crrl突变体，并确定其功能机制 通过对表达蛋白的生化分析，特别是对其进行解剖， 铜响应域。

DESCRIPTION: When chlamydomonas reinhardtii is faced with copper-deficiency, it alters the composition of a major metabolic pathway, photosynthesis, by replacing a copper protein, plastocyanin, with a heme protein, cytochrome c6. Cyt C6 is produced by transcriptional activation of the Cyc6 gene through associated copper-response elements while loss of plastocyanin is by regulated proteolysis of the apoprotein. Other adaptive processes which occur coordinately include transcriptional activation of Cpxl, encoding coproporphyrinogen oxidase - a heme biosynthesis enzyme, and Crdl, a novel diiron enzyme which is hypothesized to be involved in plastid iron mobilization, perhaps as a back-up version of a plastidlocalized, multi-copper oxidase. A copper uptake pathway involving a reductase and a transporter is also induced. Mutations at the CRR1 locus define a master regulator of copper-responsive signal transduction. This regulatory molecule appears to be involved also in the organism's response to hypoxia by serving as a Cu(II)-based redox sensor. This system provides a unique opportunity to understand and discover cellular processes occurring during copper homeostasis in the context of deficiency. In humans, copper deficiency can result from poor nutrition, especially in infants, or from genetic diseases in copper metabolism, such as Menkes disease. The objectives of this study are: 1) to deduce the function of Crdl, the putative diiron enzyme, and its homolog, Cthl, through determination of the reaction they catalyze, their sub-organellar location and pattern of expression, assessment of whether Crdl is a back-up for a copper enzyme, phenotypic analysis of crdl mutant strains, and their comparison to iron-deficient cells; 2) to understand the function of Chlamydomonas ceruloplasmins, to analyze the operation and utilization of copper enzymes in respiration vs. photosynthesis vs. iron metabolism during adaptation of C. reinhardtii to copper-deficiency, and to discover new copper-responsive targets and copper-metabolizing proteins; and 3) to identify a key regulator, Crrl, in the copper-responsive signal transduction pathway by complementation of the crrl mutant, and to determine its mechanism of function by biochemical analysis of the expressed proteins, especially dissection of its copper-responding domains.