The C. elegans CSR-1 argonaute pathway counteracts epigenetic silencing to promote germline gene expression
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UMass Chan Affiliations
Program in Molecular MedicineDocument Type
Journal ArticlePublication Date
2013-12-23Keywords
AnimalsArgonaute Proteins
Caenorhabditis elegans
Caenorhabditis elegans Proteins
*Epigenesis, Genetic
*Gene Silencing
Germ Cells
RNA Replicase
RNA, Helminth
RNA, Small Interfering
Signal Transduction
Biochemistry
Genetics and Genomics
Molecular Biology
Molecular Genetics
Metadata
Show full item recordAbstract
Organisms can develop adaptive sequence-specific immunity by reexpressing pathogen-specific small RNAs that guide gene silencing. For example, the C. elegans PIWI-Argonaute/piwi-interacting RNA (piRNA) pathway recruits RNA-dependent RNA polymerase (RdRP) to foreign sequences to amplify a transgenerational small-RNA-induced epigenetic silencing signal (termed RNAe). Here, we provide evidence that, in addition to an adaptive memory of silenced sequences, C. elegans can also develop an opposing adaptive memory of expressed/self-mRNAs. We refer to this mechanism, which can prevent or reverse RNAe, as RNA-induced epigenetic gene activation (RNAa). We show that CSR-1, which engages RdRP-amplified small RNAs complementary to germline-expressed mRNAs, is required for RNAa. We show that a transgene with RNAa activity also exhibits accumulation of cognate CSR-1 small RNAs. Our findings suggest that C. elegans adaptively acquires and maintains a transgenerational CSR-1 memory that recognizes and protects self-mRNAs, allowing piRNAs to recognize foreign sequences innately, without the need for prior exposure.Source
Seth M, Shirayama M, Gu W, Ishidate T, Conte D Jr, Mello CC. The C. elegans CSR-1 argonaute pathway counteracts epigenetic silencing to promote germline gene expression. Dev Cell. 2013 Dec 23;27(6):656-63. doi:10.1016/j.devcel.2013.11.014. Link to article on publisher's siteDOI
10.1016/j.devcel.2013.11.014Permanent Link to this Item
http://hdl.handle.net/20.500.14038/44484PubMed ID
24360782Related Resources
Link to Article in PubMedae974a485f413a2113503eed53cd6c53
10.1016/j.devcel.2013.11.014