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CHARACTERIZATION OF THE REGULATORY ROLE OF B41 GENE ON TGONDII DIFFERENTIATION

CHARACTERIZATION OF THE REGULATORY ROLE OF B41 GENE ON TGONDII DIFFERENTIATION
B41 基因对 TGONDII 分化调节作用的表征
批准号:
8168180
负责人:
MARIANA L MATRAJT
金额:
$3.84万
依托单位国家:
美国
项目类别:
财政年份:
2010
资助国家:
美国
项目状态:
已结题
起止时间:
2010-08-01 至 2011-05-31

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中文摘要
翻译
这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者(PI)可能从另一个NIH来源获得了主要资金, 因此可以在其他CRISP条目中表示。所列机构为 研究中心,而研究中心不一定是研究者所在的机构。 弓形虫是一种专性细胞内寄生虫,在温血动物中高度流行,能够感染任何有核细胞。弓形虫在人体和中间宿主中的无性繁殖有两种形式:快速生长的“速殖子”和潜伏的“缓殖子”组织包囊。速殖子是导致与先天性神经缺陷相关的急性疾病的原因,而分裂较慢的缓殖子形式可以潜伏多年,并且经常在免疫功能低下的宿主中表现出来。这两个发育阶段对于疾病的传播和致病是必不可少的。 我们已经开发了一种遗传筛选,以确定控制寄生虫分化的调控基因,并分离出在分化条件下不能转化为缓殖子的突变体。在这些突变体之一(突变体B7)中被破坏的基因座显示发育调节转录物(称为B41)的表达减少。B41不含明显的开放阅读框。我们推测,这个位点编码一个功能性的非编码RNA,在缓殖子形成中起着关键作用。我们正在进行实验,以确定这种ncRNA是否作为微小RNA的来源或作为大ncRNA的功能(这种转录物长2.6 KB,多聚腺苷酸化)。我们正在使用微阵列来研究B41和突变B7中受影响的其他基因之间可能的关系。我们正在进行实验,以功能性地表征突变体B7中被破坏的基因座。
英文摘要
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. Toxoplasma gondii is an obligate intracellular parasite, highly prevalent in warm-blooded animals and capable of infecting any nucleated cell. Two forms characterize asexual replication of Toxoplasma gondii in humans and intermediate hosts: rapidly growing 'tachyzoites' and latent 'bradyzoite' tissue cysts. Tachyzoites are responsible for acute illness that has been associated with congenital neurological defects, while the more slowly dividing bradyzoite form can remain latent for years, and often manifests itself in immunocompromised hosts. These two developmental stages are essential for disease propagation and causation. We have developed a genetic screen to identify regulatory genes that control parasite differentiation and have isolated mutants that fail to convert to bradyzoites under differentiation conditions. The locus disrupted in one of these mutants (mutant B7) shows a reduced expression of a developmentally regulated transcript, named B41. B41 contains no obvious open reading frame. We hypothesize that this locus encodes a functional non-coding RNA that plays a critical role in bradyzoite formation. We are conducting experiments to determine if this ncRNA functions as a source of micro RNAs or functions as a large ncRNA (this transcript is 2.6 KB long and polyadenylated). We are using microarrays to examine possible relationships between B41 and other genes affected in mutant B7. We are carrying out experiments to functionally characterize the disrupted locus in mutant B7.
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VERMONT COBRE: PROJECT 4: SUBVERSION OF HOST CELL SIGNALING BY TOXOPLASMA GONDII
VERMONT COBRE: PROJECT 4: SUBVERSION OF HOST CELL SIGNALING BY TOXOPLASMA GONDII
VERMONT COBRE: PROJECT 4: SUBVERSION OF HOST CELL SIGNALING BY TOXOPLASMA GONDII
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