Abstract
Double-stranded RNAs can suppress expression of homologous genes through an evolutionarily conserved process named RNA interference (RNAi) or post-transcriptional gene silencing (PTGS). One mechanism underlying silencing is degradation of target mRNAs by an RNP complex, which contains approximately 22 nt of siRNAs as guides to substrate selection. A bidentate nuclease called Dicer has been implicated as the protein responsible for siRNA production. Here we characterize the Caenorhabditis elegans ortholog of Dicer (K12H4.8; dcr-1) in vivo and in vitro. dcr-1 mutants show a defect in RNAi. Furthermore, a combination of phenotypic abnormalities and RNA analysis suggests a role for dcr-1 in a regulatory pathway comprised of small temporal RNA (let-7) and its target (e.g., lin-41).
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Alleles
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Animals
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Animals, Genetically Modified
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Caenorhabditis elegans / embryology*
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Caenorhabditis elegans / enzymology
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Caenorhabditis elegans / genetics
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DNA Primers
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Drosophila / genetics
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Embryo, Nonmammalian / physiology
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Endoribonucleases / physiology*
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Female
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GPI-Linked Proteins
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Gene Deletion
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Genes, Reporter
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Germ Cells
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Polymerase Chain Reaction
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RNA, Antisense / metabolism*
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RNA, Small Interfering
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Rabbits
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Receptors, Tumor Necrosis Factor / genetics
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Receptors, Tumor Necrosis Factor, Member 10c
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Ribonuclease III
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Tumor Necrosis Factor Decoy Receptors
Substances
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DNA Primers
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GPI-Linked Proteins
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RNA, Antisense
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RNA, Small Interfering
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Receptors, Tumor Necrosis Factor
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Receptors, Tumor Necrosis Factor, Member 10c
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TNFRSF10C protein, human
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Tumor Necrosis Factor Decoy Receptors
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Endoribonucleases
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Ribonuclease III