Molecular mechanisms of stress-induced mutation in E. coli

大肠杆菌应激突变的分子机制

• 批准号: 7911153
• 负责人: Susan M Rosenberg
• 金额: $ 24.3万
• 依托单位: BAYLOR COLLEGE OF MEDICINE
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-08-31 至 2011-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7911153
• 关键词: Address; Aging; Antibiotic Resistance; Antibiotics; Bacteria; Bacteria sigma factor KatF protein; Bacterial Chromosomes; Biological Assay; Biological Models; Cells; Cellular Stress; Chromosomes; Clinical; DNA; DNA-Directed DNA Polymerase; Double Strand Break Repair; Elements; Escherichia coli; Evolution; Generations; Genetic; Genome; Growth; Heat-Shock Response; Host Defense; Induced Mutation; Malignant Neoplasms; Mismatch Repair; Modeling; Molecular; Monobactams; Mutagenesis; Mutation; Pathway interactions; Phase; Polymerase; Production; Proteins; Regulation; Research Personnel; Resistance; Role; SECTM1 gene; Signal Transduction; Son of Sevenless Proteins; Speed; Starvation; Stress; System; Testing; Yeasts; base; biological adaptation to stress; chemotherapy; genome-wide; mutant; pathogen; programs; resistance mutation

DESCRIPTION (provided by applicant): Special mechanisms of mutation are induced in bacteria and yeasts under growth-limiting stress causing genetic instability, and occasionally, adaptive mutations that may speed evolution. These stress-induced mutation mechanisms may provide superior models for genetic changes that promote aging, genetic instability underlying cancer formation, progression and acquisition of chemotherapy resistance, resistance of pathogens to host defenses and antibiotics, and possibly much of evolution generally. This proposal focuses on understanding the molecular mechanisms of stress-induced genetic instability in an E. coli model. Because the mechanism studied has common components with several other (less understood) mechanisms of stress-induced mutation, the results should provide an important general model.

描述（由申请人提供）：在生长限制压力下，细菌和酵母中会诱导特殊的突变机制，导致遗传不稳定，偶尔也会发生可能加速进化的适应性突变。这些应激诱导的突变机制可能为促进衰老的遗传变化、癌症形成背后的遗传不稳定性、化疗耐药性的进展和获得、病原体对宿主防御和抗生素的抗性，以及可能的大部分进化提供了优越的模型。本研究的重点是了解大肠杆菌模型中应激诱导的遗传不稳定性的分子机制。由于所研究的机制与其他几种（尚不清楚的）应激诱导突变机制具有共同的成分，因此该结果应提供一个重要的通用模型。