MODE OF ACTION OF A BACTERIAL FUNCTION INVOLVED IN CELL GROWTH CONTROL

参与细胞生长控制的细菌功能的作用方式

• 批准号: 3916344
• 负责人: S GOTTESMAN
• 金额: --
• 依托单位: DIVISION OF CANCER BIOLOGY AND DIAGNOSIS
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/3916344
• 关键词: DNA repair; Escherichia coli; adenosine triphosphate; bacterial genetics; bacterial proteins; cell capsule; cell growth regulation; genetic mapping; genetic regulation; genetic transcription; genetic translation; membrane proteins; mutant; peptidases; pleiotropism; protein biosynthesis; protein sequence; proteolysis; regulatory gene

We have been studying the role that protein degradation plays in regulating cell growth control, through the study of mutants defective in ATP-dependent and independent protein turnover. E. coli lon mutants are defective in cell division regulation after DNA damage, and overproduce capsular polysaccharide. We have previously shown that an unstable positive regulator of capsule synthesis, RcsA, is stabilized in lon mutants. The rcsA function seems to be common to a number of gram-negative prokaryotes, suggesting a common mechanism for regulating different capsules in these strains. RcsC, a negative regulator of capsule synthesis, is a membrane protein which may act as a sensor for environmental signals controlling capsule synthesis. The gene for the ATP- binding subunit of a new two component ATP-dependent protease has been isolated, and chromosomal mutations in the gene, called clpA, have been generated. While cells devoid of clpA are healthy, the Clp protease seems to act as a back-up to lon in degrading abnormal proteins. A third protease function has been identified, and the gene responsible has been mapped to 56 minutes on the E. coli chromosome.

我们一直在研究蛋白质降解在 调节细胞生长控制，通过研究突变体 ATP依赖性和非依赖性蛋白质周转缺陷。 E. 大肠杆菌lon突变体在细胞分裂调节中有缺陷， DNA损伤，并产生过量的荚膜多糖。 我们有 先前表明，一个不稳定的积极调节胶囊 合成，RcsA，在lon突变体中是稳定的。 rcsA函数 似乎是许多革兰氏阴性原核生物所共有的， 这表明了调节不同胶囊的共同机制， 这些菌株。 RcsC是胶囊合成的负调节因子， 是一种膜蛋白，可以作为环境传感器 控制胶囊合成的信号。 ATP的基因- 一种新的双组分ATP依赖性蛋白酶的结合亚基， 已经被分离出来了，基因中的染色体突变，叫做clpA， 已经产生。 虽然缺乏clpA的细胞是健康的， CLP蛋白酶似乎作为一个备份，以隆在降解异常 proteins. 已经鉴定了第三种蛋白酶功能， 基因已经定位在E.杆菌 染色体