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The rde-1 gene, RNA interference, and transposon silencing in C. elegans

dc.contributor.authorTabara, Hiroaki
dc.contributor.authorSarkissian, Madathia
dc.contributor.authorKelly, William G.
dc.contributor.authorFleenor, Jamie
dc.contributor.authorGrishok, Alla
dc.contributor.authorTimmons, Lisa
dc.contributor.authorFire, Andrew Z.
dc.contributor.authorMello, Craig C.
dc.date2022-08-11T08:08:49.000
dc.date.accessioned2022-08-23T16:09:18Z
dc.date.available2022-08-23T16:09:18Z
dc.date.issued1999-10-27
dc.date.submitted2009-01-13
dc.identifier.citation<p>Cell. 1999 Oct 15;99(2):123-32.</p>
dc.identifier.issn0092-8674 (Print)
dc.identifier.doi10.1016/S0092-8674(00)81644-X
dc.identifier.pmid10535731
dc.identifier.urihttp://hdl.handle.net/20.500.14038/32660
dc.description.abstractDouble-stranded (ds) RNA can induce sequence-specific inhibition of gene function in several organisms. However, both the mechanism and the physiological role of the interference process remain mysterious. In order to study the interference process, we have selected C. elegans mutants resistant to dsRNA-mediated interference (RNAi). Two loci, rde-1 and rde-4, are defined by mutants strongly resistant to RNAi but with no obvious defects in growth or development. We show that rde-1 is a member of the piwi/sting/argonaute/zwille/eIF2C gene family conserved from plants to vertebrates. Interestingly, several, but not all, RNAi-deficient strains exhibit mobilization of the endogenous transposons. We discuss implications for the mechanism of RNAi and the possibility that one natural function of RNAi is transposon silencing.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=10535731&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.1016/S0092-8674(00)81644-X
dc.subjectAmino Acid Sequence; Animals; Animals, Genetically Modified; Caenorhabditis elegans; *Caenorhabditis elegans Proteins; Chromosomes, Artificial, Yeast; Cosmids; DNA Transposable Elements; Green Fluorescent Proteins; Helminth Proteins; Homozygote; Luminescent Proteins; Molecular Sequence Data; *Mutation; RNA, Double-Stranded; RNA, Helminth; Sequence Alignment; Sequence Homology, Amino Acid
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleThe rde-1 gene, RNA interference, and transposon silencing in C. elegans
dc.typeJournal Article
dc.source.journaltitleCell
dc.source.volume99
dc.source.issue2
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/1219
dc.identifier.contextkey693129
html.description.abstract<p>Double-stranded (ds) RNA can induce sequence-specific inhibition of gene function in several organisms. However, both the mechanism and the physiological role of the interference process remain mysterious. In order to study the interference process, we have selected C. elegans mutants resistant to dsRNA-mediated interference (RNAi). Two loci, rde-1 and rde-4, are defined by mutants strongly resistant to RNAi but with no obvious defects in growth or development. We show that rde-1 is a member of the piwi/sting/argonaute/zwille/eIF2C gene family conserved from plants to vertebrates. Interestingly, several, but not all, RNAi-deficient strains exhibit mobilization of the endogenous transposons. We discuss implications for the mechanism of RNAi and the possibility that one natural function of RNAi is transposon silencing.</p>
dc.identifier.submissionpathgsbs_sp/1219
dc.contributor.departmentProgram in Molecular Medicine
dc.contributor.departmentDepartment of Cell Biology
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.source.pages123-32


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