dicer
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a multidomain endonuclease of ribonuclease III-type that is involved in the generation of small interfering RNAs (siRNA) and other forms of microRNA (miRNA) species. It is important for normal development in Caenorhabditis elegans. The human and Drosophila enzymes are homologous and contain a DEXH-box ATP-dependent RNA helicase domain, tandem RNase III motifs, and a C-terminal dsRNA-binding domain. In animals, Dicer and its cofactors are absent in differentiated cells.
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Dicer is an endoribonuclease in the RNase III family that cleaves double-stranded RNA (dsRNA) and pre-microRNA (miRNA) into short double-stranded RNA fragments called small interfering RNA (siRNA) about 20-25 nucleotides long, usually with a two-base overhang on the 3' end. Dicer contains two RNase III domains and one PAZ domain; the distance between these two regions of the molecule is determined by the length and angle of the connector helix and may influence the length of the siRNAs it produces.[1] Dicers interact with several partner proteins (TRBP in humans, R2D2, Loqs in Drosophila). These partner proteins could play a role in dictating the substrate specificity of Dicer proteins.[2]
Dicer facilitates the formation of the RNA-induced silencing complex (RISC), whose catalytic component argonaute is an endonuclease capable of degrading messenger RNA (mRNA). The human version of this gene is DICER1.
Dicer and other miRNA processing enzymes may be important in cancer prognosis.[3] When researchers in British Columbia sequenced the genomes of rare ovarian, uterine, and testicular tumours, they have found that the same fundamental mutation in the DICER gene showed up as the common process underlying all of the different cancers they have examined. The DICER gene regulates the development and behavior of normal cells in the body, and the mutation of this gene causes this regulating ability to be warped, producing cancerous cells. [4]
History
Dicer was given its name by Emily Bernstein, a graduate student in Greg Hannon's lab at Cold Spring Harbor Laboratory, who first demonstrated the enzyme's dsRNA "dicing" activity.[5]
In the moss Physcomitrella patens DCL1b, one of four DICER proteins, is not involved in miRNA biogenesis but in dicing miRNA target transcripts. Thus, a novel mechanism for regulation of gene expression, the epigenetic silencing of genes by miRNAs, was discovered.[6][7]
References
- ^ a b Macrae I, Zhou K, Li F, Repic A, Brooks A, Cande W, Adams P, Doudna J (2006). "Structural basis for double-stranded RNA processing by Dicer". Science 311 (5758): 195–8. doi:10.1126/science.1121638. PMID 16410517.
- ^ Cenik ES, ..., Zamore PD (2011). "Phosphate and R2D2 restrict the substrate specificity of Dicer-2, an ATP-driven ribonuclease". Molecular Cell 42 (2): 172–84. doi:10.1016/j.molcel.2011.03.002. PMID 21419681.
- ^ Slack FJ and Weidhaas JB. MicroRNA in cancer prognosis. New England Journal of Medicine 359 (25):2720-2722
- ^ University of British Columbia. "Single gene links rare and unrelated cancers". Medical Xpress. http://medicalxpress.com/news/2011-12-gene-links-rare-unrelated-cancers.html
- ^ Bernstein E, Caudy A, Hammond S, Hannon G (2001). "Role for a bidentate ribonuclease in the initiation step of RNA interference". Nature 409 (6818): 363–6. doi:10.1038/35053110. PMID 11201747.
- ^ B. Khraiwesh, M.A. Arif, G.I. Seumel, S. Ossowski, D. Weigel, R. Reski , W. Frank (2010): Transcriptional Control of Gene Expression by MicroRNAs. Cell 140,111-122.doi:10.1016/j.cell.2009.12.023
- ^ Discovery: microRNAs can directly turn off genes
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