Dicer-1 and R3D1-L catalyze microRNA maturation in Drosophila
Dicer-1 and R3D1-L catalyze microRNA maturation in Drosophila
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DOI：
10.1101/gad.1334005
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发表时间：
2005-07-15
影响因子：
10.5
通讯作者：
Liu, QH
中科院分区：
文献类型：
--
作者：
Jiang, F;Ye, XC;Liu, QH
Drosophila melanogaster、Dicer-2/R2132和Dicer-1分别产生小干扰RNA（siRNA）和微小RNA（miRNA）。在这里，我们确定了一个新的dsRNA结合蛋白，我们命名为R3 D1-L，形成一个稳定的复合物与Dicer-1在体外和体内。虽然通过RNAi耗尽R3 D1-L导致前体miRNA（pre-miRNA）在S2细胞中积累，但重组R3 D1-L在体外增强Dicer-1的miRNA产生。此外，R3 D1缺陷导致雄性和雌性果蝇的miRNA产生缺陷和严重的不育。因此，R3 D1-L在miRNA生物合成中与Dicer-1协同作用，并且是果蝇生殖发育所必需的。
Drosophila melanogaster, Dicer-2/R2132 and Dicer-1 generate small interfering RNA (siRNA) and microRNA (miRNA), respectively. Here we identify a novel dsRNA-binding protein, which we named R3D1-L, that forms a stable complex with Dicer-1 in vitro and in vivo. While depletion of R3D1-L by RNAi causes accumulation of precursor miRNA (pre-miRNA) in S2 cells, recombinant R3D1-L, enhances miRNA production by Dicer-1 in vitro. Furthermore, R3D1 deficiency causes miRNA-generating defect and severe sterility in male and female flies. Therefore, R3D1-L functions in concert with Dicer-1 in miRNA biogenesis and is required for reproductive development in Drosophila.