Inhibition of Plasmodium falciparum clag9 gene function by antisense RNA
Inhibition of Plasmodium falciparum clag9 gene function by antisense RNA
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DOI：
10.1016/s0166-6851(00)00254-1
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发表时间：
2000-09-01
影响因子：
1.5
通讯作者：
Trenholme, KR
中科院分区：
文献类型：
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作者：
Gardiner, DL;Holt, DC;Trenholme, KR
我们以前已经表明，通过靶向基因破坏，恶性疟原虫的clag9基因是必不可少的细胞粘附CD36。在这里，我们报告的抑制clag9的功能，通过使用反义RNA载体作为替代靶向基因破坏。我们将clag9的反义构建体转染到恶性疟原虫克隆3D7中，并且当在乙胺嘧啶存在下培养所得到的细胞系时，其显示出比对照低15倍的对C32黑素瘤细胞的细胞粘附。在去除引入的质粒后回复到野生型提供了直接证据，表明引起表型变化的事件不在不相关的位点，并且这种方法在疟疾转染技术中提供了有价值的新工具。(C)2000 Elsevier Science B.V.保留所有权利。
We have previously shown by targeted gene disruption that the clag9 gene of Plasmodium falciparum is essential for cytoadherence to CD36. Here we report inhibition of the function of clag9 by the use of an antisense RNA vector as an alternative to targeted gene disruption. We transfected an antisense construct of clag9 into the P. falciparum clone 3D7 and when the resulting line was cultured in the presence of pyrimethamine it showed 15-fold lower cytoadherence to C32 melanoma cells than the control. Reversion to wildtype upon removal of the introduced plasmid provides direct evidence that the event responsible for the phenotypic change is not at an unrelated site and this approach provides a valuable new tool in malaria transfection technology. (C) 2000 Elsevier Science B.V. All rights reserved.