BIOLOGICAL VARIATION AMONG AFRICAN TRYPANOSOMES

非洲锥虫的生物学变异

• 批准号: 6349827
• 负责人: John M. Mansfield
• 金额: $ 25.75万
• 依托单位: UNIVERSITY OF WISCONSIN-MADISON
• 依托单位国家: 美国
• 财政年份: 2000
• 资助国家: 美国
• 起止时间: 2000-02-15 至 2003-01-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6349827
• 关键词: Cercopithecidae; Trypanosoma brucei rhodesiense; biomarker; complementary DNA; gene expression; gene targeting; laboratory mouse; molecular cloning; northern blottings; nuclear runoff assay; nucleic acid sequence; pathologic process; phenotype; polymerase chain reaction; pulsed field gel electrophoresis; restriction fragment length polymorphism; southern blotting; tissue /cell culture; transfection; virulence

DESCRIPTION (Adapted from the Applicant's Abstract): This is a new R21 from Dr. Mansfield that aims to determine the basis for virulence in African trypanosomes. The proposed research would extend studies originally funded in a one year RO3 award, made in 1997 but extended to two years via a no-cost extension. The aims of the previous proposal are essentially unchanged in this one, however, additional progress is reported. Dr. Mansfield hypothesizes that virulence may be controlled by a rheostat-like mechanism involving differentially expressed virulence genes (or genes that inhibit virulence). There are two specific aims: first to identify differentially transcribed mRNAs and synthesized proteins in genetically related members of the LouTat 1 clone of Trypanosoma brucei rhodesiense and to characterize the genomic organization of these genes. Second, the role of these genes in virulence would be confirmed by genetic manipulation of trypanosomes using gene complementation, disruption and over expression.

描述（改编自申请人的摘要）：这是来自Dr. 曼斯菲尔德，旨在确定非洲的毒力基础， 锥虫拟议的研究将扩展最初资助的研究， 一年RO3奖，1997年，但延长到两年，通过免费 扩展名.上一个提案的目的在这方面基本不变。 然而，据报道，还有一项额外的进展。曼斯菲尔德医生假设 毒力可能是由一种类似变阻器的机制控制的， 差异表达的毒力基因（或抑制毒力的基因）。 有两个具体的目标：第一，确定差异转录的mRNA 并在LouTat 1克隆的遗传相关成员中合成蛋白质 布氏锥虫罗得西亚亚种的基因组结构特征 这些基因。其次，这些基因在毒力中的作用将得到证实 通过使用基因互补、破坏 和过度表达