Analysis of short RNAs in the malaria parasite and its red blood cell host
Analysis of short RNAs in the malaria parasite and its red blood cell host
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DOI：
10.1016/j.febslet.2006.08.063
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发表时间：
2006-10-02
期刊：
影响因子：
3.5
通讯作者：
Dalmay, Tamas
中科院分区：
文献类型：
--
作者：
Rathjen, Tina;Nicol, Clare;Dalmay, Tamas
RNA干扰（RNAi）是一种RNA降解过程，涉及短的双链RNA（dsRNA）作为序列特异性因子。RNAi机制的天然功能是产生内源性短双链RNA以调节基因表达。已经显示，用dsRNA治疗恶性疟原虫（疟疾的病原体）诱导相应的微小RNA（miRNA）降解，然而在寄生虫基因组中尚未鉴定出典型的RNAi相关基因。为了澄清这种差异，我们着手从恶性疟原虫感染的红细胞和纯化的寄生虫中克隆短RNA。我们没有发现任何不是rRNA或tRNA片段的短RNA。实际上，在寄生虫制备物中仅分离出已知的人miRNA，这表明在恶性疟原虫中存在非常少的短RNA（如果有的话）。这表明在观察dsRNA介导的降解中存在与经典RNAi不同的机制。在鉴定的人miRNA中，人miRNA mir-451在感染和健康红细胞中以非常高的水平积累。有趣的是，在代表所有主要血液谱系的祖细胞阶段的一系列永生化细胞系中检测不到mir-451，这表明mir-451可能在红系细胞的分化中起作用。(c)2006年欧洲生物化学学会联合会。Elsevier B. V.出版，保留所有权利。
RNA interference (RNAi) is an RNA degradation process that involves short, double-stranded RNAs (dsRNA) as sequence specificity factors. The natural function of the RNAi machinery is to generate endogenous short double-stranded RNAs to regulate gene expression. It has been shown that treatment of Plasmodium falciparum, the etiologic agent of malaria, with dsRNA induces degradation of the corresponding microRNA (miRNA), yet typical RNAi-associated genes have not been identifiable in the parasite genome. To clarify this discrepancy we set out to clone short RNAs from P. falciparum-infected red blood cells and from purified parasites. We did not find any short RNA that was not a rRNA or tRNA fragment. Indeed, only known human miRNAs were isolated in parasite preparations indicating that very few if any short RNAs exist in P. falciparum. This suggests a different mechanism than classical RNAi in observations of dsRNA-mediated degradation. Of the human miRNAs identified, the human miRNA mir-451 accumulates at a very high level in both infected and healthy red blood cells. Interestingly, mir-451 was not detectable in a series of immortalised cell lines representing progenitor stages of all major blood lineages, suggesting that mir-451 may play a role in the differentiation of erythroid cells. (c) 2006 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.