CHARACTERIZATION OF THE DISRUPTED LOCUS IN A TOXOPLASMA GONDII BRADYZOITE DIFFER

本子项目是利用由NIH/NCRR资助的中心赠款提供的资源的众多研究子项目之一。子项目和研究者（PI）可能已经从另一个NIH来源获得了主要资金，因此可以在其他CRISP条目中表示。列出的机构是中心的，不一定是研究者的机构。人类病原体刚地弓形虫是分布最广泛的原生动物寄生虫之一，感染了世界上大约三分之一的地区。年代人口。弓形虫无性繁殖有两种特征；快速生长？速殖子？潜伏的？缓殖子？组织囊肿。这两个发育阶段是疾病传播和病因的核心。快殖子和慢殖子之间的相互转化是寄生虫生存和致病性的核心，但在分子和遗传水平上却知之甚少，这使得理解这一过程成为一个重要的目标。最近，人们开发了一种基因筛选方法来鉴定控制寄生虫分化的调控基因，并分离出了在分化条件下无法转化为慢殖子的突变体。其中一个突变体（突变体B7）的断裂位点已被确定，并且在突变体寄生虫中发育调控转录物（B41）的表达已被取消。B41被转录；然而，它没有包含明显的开放阅读框架。该项目的目标是对突变体B7中被破坏的基因座进行功能表征，并验证该基因座编码在慢殖子形成中起关键作用的功能性非编码RNA的假设。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The human pathogen Toxoplasma gondii is one of the most widely distributed protozoan parasites, infecting approximately one-third of the world?s population. Two forms characterize asexual reproduction of T. gondii; rapidly growing ?tachyzoites? and latent ?bradyzoite? tissue cysts. These two developmental stages are central to disease propagation and causation. The interconversion between tachyzoites and bradyzoites, at the heart of parasite survival and pathogenicity, is poorly understood at a molecular and genetic level, which makes understanding this process an important goal. Recently, a genetic screen was developed to identify regulatory genes that control parasite differentiation and mutants that fail to convert to bradyzoites under differentiation conditions have been isolated. The disrupted locus in one of these mutants (mutant B7) has been identified and the expression of a developmentally regulated transcript (B41) has been abolished in the mutant parasites. B41 is transcribed; yet it contains no obvious open reading frame. The goal of this project is to functionally characterize the disrupted locus in the mutant B7 and test the hypothesis that this locus codes for a functional non-coding RNA that plays a critical role in bradyzoite formation.