Transcriptional Regulation in Plasmodium falciparum

描述（由申请方提供）：人类疟疾由感染引起 由原生动物寄生虫疟原虫属。目前，3亿至5亿人 每年有150万至350万人死于疟疾， 疾病虽然许多恶性疟原虫基因的表达参与了 发病机制和发展在转录水平上受到调节， 几乎没有关于这些生物体中转录的机制信息。 因此，三个恶性疟原虫热休克基因的转录将被分析为 一个模型系统将使用核运行分析来确定 这些基因的转录速率在不存在和存在的热应激。 将使用体内报告基因测定来确定启动子序列 需要转录。需要转录热量的蛋白质 休克基因将通过DNA亲和层析纯化，并通过 质谱法这些研究将增进我们对 转录在恶性疟原虫，并允许更好地了解 致病机制，分化和耐药性在这种寄生虫。

DESCRIPTION (provided by the applicant): Human malaria results from infection by the protozoan parasite Plasmodium sp. Currently, 300-500 million peoples are infected with malaria, and 1.5-3.5 million individuals succumb annually to the disease. Although expression of many P. falciparum genes involved in pathogenesis and development are regulated at the level of transcription, there is little mechanistic information regarding transcription in these organisms. Thus, transcription of three P. falciparum heat shock genes will be analyzed as a model system. Nuclear run on assays will be used to determine the transcription rates of these genes in the absence and presence of heat stress. In vivo reporter assays will be used to determine the promoter sequences required for transcription. Proteins that require transcription of the heat shock genes will be purified by DNA affinity chromatography and identified by mass spectroscopy. These studies will enhance our understanding of transcription in P. falciparum, and allow a better understanding of pathogenesis, differentiation, and drug resistance in this parasite.