Restricted and non-essential redundancy of RNAi and piRNA pathways in mouse oocytes
Jazyk angličtina Země Spojené státy americké Médium electronic-ecollection
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
31860668
PubMed Central
PMC6944382
DOI
10.1371/journal.pgen.1008261
PII: PGENETICS-D-19-00984
Knihovny.cz E-zdroje
- MeSH
- Argonaut proteiny genetika MeSH
- DEAD-box RNA-helikasy genetika MeSH
- malá interferující RNA genetika MeSH
- mutace MeSH
- myši MeSH
- oocyty chemie růst a vývoj MeSH
- retroelementy * MeSH
- ribonukleasa III genetika MeSH
- RNA interference * MeSH
- signální transdukce MeSH
- zvířata MeSH
- Check Tag
- myši MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- Argonaut proteiny MeSH
- DEAD-box RNA-helikasy MeSH
- Dicer1 protein, mouse MeSH Prohlížeč
- malá interferující RNA MeSH
- Piwil2 protein, mouse MeSH Prohlížeč
- retroelementy * MeSH
- ribonukleasa III MeSH
Germline genome defense evolves to recognize and suppress retrotransposons. One of defensive mechanisms is the PIWI-associated RNA (piRNA) pathway, which employs small RNAs for sequence-specific repression. The loss of the piRNA pathway in mice causes male sterility while females remain fertile. Unlike spermatogenic cells, mouse oocytes posses also RNA interference (RNAi), another small RNA pathway capable of retrotransposon suppression. To examine whether RNAi compensates the loss of the piRNA pathway, we produced a new RNAi pathway mutant DicerSOM and crossed it with a catalytically-dead mutant of Mili, an essential piRNA gene. Normal follicular and oocyte development in double mutants showed that RNAi does not suppress a strong ovarian piRNA knock-out phenotype. However, we observed redundant and non-redundant targeting of specific retrotransposon families illustrating stochasticity of recognition and targeting of invading retrotransposons. Intracisternal A Particle retrotransposon was mainly targeted by the piRNA pathway, MaLR and RLTR10 retrotransposons were targeted mainly by RNAi. Double mutants showed accumulations of LINE-1 retrotransposon transcripts. However, we did not find strong evidence for transcriptional activation and mobilization of retrotransposition competent LINE-1 elements suggesting that while both defense pathways are simultaneously expendable for ovarian oocyte development, yet another transcriptional silencing mechanism prevents mobilization of LINE-1 elements.
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