COPPER-RESPONSIVE SIGNAL TRANSDUCTION

描述：当莱茵衣藻面临缺铜时，它 改变主要代谢途径的组成，光合作用，通过 用一种细胞色素C6来代替铜蛋白，即胞质蓝蛋白。 细胞色素C6是通过转录激活Cyc6基因而产生的 相关的铜响应元件，而塑料蓝蛋白的损失是受调控的 脱辅基蛋白的蛋白分解。发生的其他适应性过程 协同包括Cpx1的转录激活，编码 一种新的血红素生物合成酶--辅酶A氧化酶和CRDL 一种被认为与叶绿体铁有关的二铁酶 动员，也许是塑料的备份版本，本地化，多铜 氧化物酶。一个涉及还原酶和转运体的铜吸收途径是 也是被诱导的。CRR1基因座的突变定义了一个主要的调节因子 铜反应信号转导。这种调节分子似乎是 也参与有机体对低氧的反应，作为一种 基于铜(II)的氧化还原传感器。这一系统提供了一个独特的机会 了解和发现铜稳态过程中的细胞过程 在不足的情况下。在人类中，贫穷可能导致铜缺乏。 营养，特别是婴儿的营养，或铜的遗传病 新陈代谢，如门克斯病。这项研究的目标是：1) 推测可能的二铁酶CRDl及其同源物Cthl， 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是否为 铜酶、CRDl突变株的表型分析和它们的 与缺铁细胞比较；2)了解铁缺乏细胞的功能 铜绿假单胞菌的经营利用分析 呼吸作用中的铜酶与光合作用与铁代谢 莱茵红曲霉对缺铜的适应及新发现 铜反应靶标和铜代谢蛋白；3)识别 铜反应信号转导通路中的关键调节因子CRRL通过 CRRL突变体的互补作用及其作用机制的研究 通过对表达的蛋白质进行生化分析，特别是对其 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.