GSE132121
Analysis of redundancy between RNAi and piRNA pathways in the mouse oocytes
Suppression of retrotransposons is an integral part of germline genome defense. The PIWI-associated RNA (piRNA) pathway mediates post-transcriptional and transcriptional silencing of retrotransposons in vertebrates. The loss of the piRNA pathway in mice results in male sterility while females remain fertile. Unlike spermatogenic cells, mouse oocytes utilize also RNA interference (RNAi) pathway, another small RNA pathway capable of retrotransposon suppression. To examine redundancy of piRNA and RNAi pathway in the mouse female germline, we produced an RNAi pathway mutant DicerSOM and crossed it with a catalytically-dead mutant of Mili, an essential piRNA factor. Ovaries and follicular development in mice lacking both pathways appear normal suggesting that RNAi in oocytes does not rescue a piRNA pathway knock-out phenotype. We observed that one of the pathways dominates in suppression of different retrotransposons. Intracisternal A Particle retrotransposon is mainly targeted by the piRNA pathway, MT and RLTR10 retrotransposons were targeted mainly by RNAi. Importantly, both pathways redundantly suppress LINE-1 retrotransposons where the loss of both RNA silencing pathways yielded ~6-fold upregulation of negligible levels of LINE-1 transcripts. This implies that another transcriptional silencing mechanism must contribute to LINE-1 repression and could explain why both, RNAi and piRNA pathways, are non-essential defense pathway in the mouse female germline. Overall design: We report transcriptome profiles of partial and complete knockout of Dicer1 specific isoform in oocytes.