A retrotransposon-driven dicer isoform directs endogenous small interfering RNA production in mouse oocytes
Language English Country United States Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
24209619
DOI
10.1016/j.cell.2013.10.001
PII: S0092-8674(13)01228-2
Knihovny.cz E-resources
- MeSH
- DEAD-box RNA Helicases chemistry genetics metabolism MeSH
- Gene Expression MeSH
- Phylogeny MeSH
- RNA, Small Interfering chemistry metabolism MeSH
- Molecular Sequence Data MeSH
- Mice MeSH
- Oocytes metabolism MeSH
- Promoter Regions, Genetic MeSH
- Protein Isoforms chemistry genetics metabolism MeSH
- Retroelements * MeSH
- Ribonuclease III chemistry genetics metabolism MeSH
- Base Sequence MeSH
- Infertility, Female MeSH
- Animals MeSH
- Check Tag
- Mice MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- DEAD-box RNA Helicases MeSH
- Dicer1 protein, mouse MeSH Browser
- RNA, Small Interfering MeSH
- Protein Isoforms MeSH
- Retroelements * MeSH
- Ribonuclease III MeSH
In mammals, a single Dicer participates in biogenesis of small RNAs in microRNA (miRNA) and RNAi pathways. In mice, endogenous RNAi is highly active in oocytes, but not in somatic cells, which we ascribe here to an oocyte-specific Dicer isoform (Dicer(O)). Dicer(O) lacks the N-terminal DExD helicase domain and has higher cleavage activity than the full-length Dicer in somatic cells (Dicer(S)). Unlike Dicer(S), Dicer(O) efficiently produces small RNAs from long double-stranded (dsRNA) substrates. Expression of the Dicer(O) isoform is driven by an intronic MT-C retrotransposon promoter, deletion of which causes loss of Dicer(O) and female sterility. Oocytes from females lacking the MT-C element show meiotic spindle defects and increased levels of endogenous small interfering RNA (endo-siRNA) targets, phenocopying the maternal Dicer null phenotype. The alternative Dicer isoform, whose phylogenetic origin demonstrates evolutionary plasticity of RNA-silencing pathways, is the main determinant of endogenous RNAi activity in the mouse female germline.
References provided by Crossref.org
Enhanced RNAi does not provide efficient innate antiviral immunity in mice
PIWI-interacting RNAs: who, what, when, where, why, and how
DDI2 protease controls embryonic development and inflammation via TCF11/NRF1
Functional canonical RNAi in mice expressing a truncated Dicer isoform and long dsRNA
Dicer structure and function: conserved and evolving features
De novo emergence, existence, and demise of a protein-coding gene in murids
Structural and functional basis of mammalian microRNA biogenesis by Dicer
Formation of spermatogonia and fertile oocytes in golden hamsters requires piRNAs
CRISPR-Induced Expression of N-Terminally Truncated Dicer in Mouse Cells
MicroRNA dilution during oocyte growth disables the microRNA pathway in mammalian oocytes
Restricted and non-essential redundancy of RNAi and piRNA pathways in mouse oocytes
Main constraints for RNAi induced by expressed long dsRNA in mouse cells
Role of Cnot6l in maternal mRNA turnover
The oocyte-to-embryo transition in mouse: past, present, and future
Alternative intronic promoters in development and disease
Long non-coding RNA exchange during the oocyte-to-embryo transition in mice
KLK5 and KLK7 Ablation Fully Rescues Lethality of Netherton Syndrome-Like Phenotype
Production of small RNAs by mammalian Dicer
GEO
GSE41207
