GENE CONTROL IN INFECTION AND LYSOGENY BY PHAGE LAMBDA

噬菌体 Lambda 对感染和溶原的基因控制

• 批准号: 2765453
• 负责人: JEFFREY W ROBERTS
• 金额: $ 55.77万
• 依托单位: CORNELL UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 1978
• 资助国家: 美国
• 起止时间: 1978-02-01 至 2004-01-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2765453
• 关键词: DNA binding protein; DNA directed RNA polymerase; DNA footprinting; Escherichia coli; bacterial DNA; bacterial genetics; bacteriophage lambda; binding sites; crosslink; enzyme mechanism; gene mutation; genetic regulation; genetic transcription; intermolecular interaction; lysogeny; protein structure function; transcription factor; transcription termination; virus infection mechanism; virus protein

DESCRIPTION (adapted from the investigator's abstract): Gene expression in normal and pathological conditions is mediated by RNA polymerase enzymes, a family of complex, multisubunit molecular machines that is highly conserved in evolution. RNA polymerase function is controlled not only at the level of access to genes (transcription initiation), but also during enzyme progression as RNAP carries out its sequential readout of the gene message. An important example of such control occurs in HIV virus and is mediated by its major regulator, the TAT gene. The central models for understanding enzymatic mechanisms involved in transcriptional regulation are the antitermination proteins of the E. coli bacteriophage lambda, the Q protein, which modifies RNA polymerase near its initiation site, but then becomes a subunit of the enzyme, allowing it to elongate more efficiently and to progress through transcription termination signals. The investigator will study important elements of both the Q polypeptide and the subunits of RNA polymerase that are required for their physical and functional interaction, particularly the sigma initiation factor which mediates the initial engagement of Q protein with RNA polymerase, and he will examine the altered enzymatic properties of Q modified RNA polymerase. He will investigate the mechanism of transcription termination and the manner in which regulatory proteins interfere with this process.

描述（根据研究者的摘要改编）：基因表达 在正常和病理条件下，由RNA聚合酶介导 酶，一个复杂的多亚基分子机器的家族，是 高度保守进化。 RNA聚合酶功能不受控制 仅在获得基因的访问水平（转录启动），但 当RNAP执行其顺序时，酶进展过程中也是 读数基因消息。发生这种控制的一个重要例子发生 在HIV病毒中，由其主要调节剂TAT基因介导。这 理解涉及酶机制的中心模型 转录调节是E的抗授权蛋白。 大肠菌噬菌体lambda，Q蛋白，可修饰RNA聚合酶 在其启动位置附近，但随后成为酶的亚基， 允许它更有效地伸长并通过 转录终止信号。研究人员将研究重要 Q多肽和RNA聚合酶亚基的元素 它们的身体和功能相互作用所需的是 特别是介导初始的Sigma启动因子 Q蛋白与RNA聚合酶的参与，他将检查 Q修饰的RNA聚合酶的酶特性改变。他会的 研究转录终止的机制和方式 其中调节蛋白会干扰此过程。