A Cellular Function for the RNA-Interference Enzyme Dicer in the Maturation of the let-7 Small Temporal RNA

American Association for the Advancement of Science (AAAS) - Tập 293 Số 5531 - Trang 834-838 - 2001
György Hutvágner1, Juanita McLachlan2, Amy E. Pasquinelli3, Éva Bálint4, Thomas Tuschl5, Phillip D. Zamore2
1Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, MA, 01655, USA
2Department of Biochemistry and Molecular Pharmacology
3Department of Molecular Biology, Massachusetts General Hospital and Department of Genetics, Harvard Medical School, Boston, MA 02114 USA
4Department of Cell Biology, University of Massachusetts Medical School, Worcester MA 01655, USA
5Department of Cellular Biochemistry, Max-Planck-Institute for Biophysical Chemistry, Am Fassberg 11, D-37077 Go ¨ttingen, Germany

Tóm tắt

The 21-nucleotide small temporal RNA (stRNA) let-7 regulates developmental timing in Caenorhabditis elegans and probably in other bilateral animals. We present in vivo and in vitro evidence that in Drosophila melanogaster a developmentally regulated precursor RNA is cleaved by an RNA interference-like mechanism to produce mature let-7 stRNA. Targeted destruction in cultured human cells of the messenger RNA encoding the enzyme Dicer, which acts in the RNA interference pathway, leads to accumulation of the let-7 precursor. Thus, the RNA interference and stRNA pathways intersect. Both pathways require the RNA-processing enzyme Dicer to produce the active small-RNA component that represses gene expression.

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Tài liệu tham khảo

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We thank A. Grishok C. Mello and G. Ruvkun for sharing data before publication; G. Stein for providing facilities for HeLa cell culture; and D. Bartel A. Grishok K. Knight C. Mello G. Ruvkun P. Sharp F. Slack and members of the Zamore laboratory for discussions and comments on the manuscript. We acknowledge A. Grishok and C. Mello for the suggestion that pre- let-7 hairpins might be engineered to generate non- let-7 products. P.D.Z. is a Pew Scholar in the Biomedical Sciences. Supported in part by a grant from the NIH (GM62862-01) to P.D.Z.