Knight Scott W, Bass Brenda L
Department of Biochemistry and Howard Hughes Medical Institute, University of Utah, 20 North 1900 East, Salt Lake City, UT 84132, USA.
Mol Cell. 2002 Oct;10(4):809-17. doi: 10.1016/s1097-2765(02)00649-4.
Adenosine deaminases that act on RNA (ADARs) are RNA-editing enzymes that deaminate adenosines to create inosines in double-stranded RNA (dsRNA). Here we demonstrate that ADARs are not required for RNA interference (RNAi) and that they do not antagonize the pathway to a detectable level when RNAi is initiated by injecting dsRNA. We find, however, that transgenes expressed in the somatic tissues of wild-type animals are silenced in strains with deletions in the two genes encoding ADARs, adr-1 and adr-2. Transgene-induced gene silencing in adr-1;adr-2 mutants depends on genes required for RNAi, suggesting that a dsRNA intermediate is involved. In wild-type animals we detect edited dsRNA corresponding to transgenes, and we propose that editing of this dsRNA prevents somatic transgenes from initiating RNAi in wild-type animals.
作用于RNA的腺苷脱氨酶（ADARs）是一种RNA编辑酶，可将腺苷脱氨基，在双链RNA（dsRNA）中产生肌苷。在这里，我们证明RNA干扰（RNAi）并不需要ADARs，并且当通过注射dsRNA启动RNAi时，它们不会将该途径拮抗到可检测的水平。然而，我们发现，在野生型动物的体细胞组织中表达的转基因，在编码ADARs的两个基因adr-1和adr-2缺失的菌株中会被沉默。adr-1；adr-2突变体中的转基因诱导基因沉默取决于RNAi所需的基因，这表明涉及dsRNA中间体。在野生型动物中，我们检测到与转基因相对应的编辑后的dsRNA，并且我们提出这种dsRNA的编辑可防止野生型动物中的体细胞转基因启动RNAi。
