Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA289872 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2102030.fastq.gz | Fastqsanger.gz | |||
| SRR2102028.fastq.gz | Fastqsanger.gz | |||
| SRR2102029.fastq.gz | Fastqsanger.gz |
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Project description:Mammalian genomes harbor millions of retrotransposon copies, some of which are transpositionally active. In mouse prospermatogonia, PIWI-interacting small RNAs called piRNAs combat retrotransposon activity. The piRNA system guides de novo DNA methylation at retrotransposon promoters, but it remains unclear whether DNA methylation is involved in retrotransposon silencing in prospermatogonia. We performed a genome-wide study of DNA methylation and RNA abundance for retrotransposons in developing mouse male germ cells, using Pld6/Mitopld and Dnmt3l knockout (KO) mice deficient in piRNA biogenesis and de novo DNA methylation, respectively. The Dnmt3l mutation greatly reduced DNA methylation at most retrotransposons but its effect on their RNA abundance was low in prospermatogonia. In the Pld6 mutants, only few retrotransposons exhibited reduced DNA methylation but many were more upregulated at the RNA level than in the Dnmt3l mutants. Moreover, the retrotransposon upregulation by the Pld6 mutation was observed even in the Dnmt3l KO background. Thus, in prospermatogonia, post-transcriptional RNA digestion by the piRNA system plays a more important role in retrotransposon regulation than transcriptional silencing by DNA methylation. However, their relative importance was changed in meiotic spermatocytes where hypomethylation of retrotransposons increased their expression by up to 100-fold in both mutants. Interestingly, retrotransposon activation disrupted the transcriptome integrity because intergenic and intronic retrotransposon sequences, in particular, the antisense promoter of LINE-1, drive expression of nearby genes.
2017-07-20 | GSE70891 | GEO
Project description:In the male germline of mammals, the expression of retrotransposons is restricted by DNA methylation, trimethylation of histone H3 at lysin-9 (H3K9me3) and PIWI-interacting small RNAs (piRNAs). To elucidate their relative importance in regulating retrotransposons during germ-cell development as well as relationships between these mechanisms, we performed mRNA, DNA methylation, and histone methylation analyses using mouse spermatogonia from Dnmt3l and Pld6 mutants deficient in de novo DNA methylation and piRNA production, respectively. The results revealed that a loss of DNA methylation results in decreased H3K9me3 and increased H3K4me3, suggesting a pivotal role of DNA methylation in maintaining the epigenome integrity.
2025-12-04 | GSE296268 | GEO
Project description:In the male germline of mammals, the expression of retrotransposons is restricted by DNA methylation, trimethylation of histone H3 at lysin-9 (H3K9me3) and PIWI-interacting small RNAs (piRNAs). To elucidate their relative importance in regulating retrotransposons during germ-cell development as well as relationships between these mechanisms, we performed mRNA, DNA methylation, and histone methylation analyses using mouse spermatogonia from Dnmt3l and Pld6 mutants deficient in de novo DNA methylation and piRNA production, respectively. The results revealed that a loss of DNA methylation results in decreased H3K9me3 and increased H3K4me3, suggesting a pivotal role of DNA methylation in maintaining the epigenome integrity.
2025-12-04 | GSE296267 | GEO
Project description:We used RRBS to analyze DNA methylation in mESC lines deficient for maternal Dnmt3L (Dnmt3L mKO), zygotic Dnmt3L (Dnmt3L KO), and both maternal and zygotic Dnmt3L (Dnmt3L mzKO). Compared to wild-type (WT) mESCs, Dnmt3L mKO mESCs exhibit severe loss of methylation at imprinted loci but no changes in global DNA methylation, Dnmt3L KO mESCs exhibit moderate loss of methylation at many Dnmt3a target regions but do not affect methylation at imprinted loci, and Dnmt3L mzKO mESCs exhibit combined changes of mKO and KO cells, with severe loss of methylation at imprinted loci and moderate loss of methylation at Dnmt3a target regions.
2018-10-04 | GSE116489 | GEO
Project description:In the male germline of mammals, retrotransposon expression is restricted by DNA methylation, trimethylation of histone H3 at lysin-9 (H3K9me3), and PIWI-interacting small RNAs (piRNAs). To elucidate their relative importance in regulating retrotransposons during germ cell development and the relationships between these mechanisms, we performed mRNA, DNA methylation, and histone methylation analyses using mouse spermatogonia from Dnmt3l and Pld6 mutants deficient in de novo DNA methylation and piRNA production, respectively. The results revealed that loss of DNA methylation resulted in decreased H3K9me3 in young L1 subfamilies and increased H3K4me3 in many retrotransposons, suggesting a pivotal role of DNA methylation in maintaining epigenomic integrity in spermatogonia and later stages of spermatogenesis. The transcriptional upregulation of retrotransposons by a loss of DNA methylation was more evident during meiosis (spermatocytes) than before meiosis (spermatogonia). These results are aligned with a global reduction of H3K9me3 at retrotransposons in spermatocytes. The piRNA system also regulated H3K9me3 and H3K4me3 at retrotransposons in spermatogonia likely through the regulation of DNA methylation, since the loss of DNA methylation resulted in decreased H3K9me3 and increased H3K4me3 at the same retrotransposon loci even in the presence of piRNAs.
2025-12-04 | GSE296269 | GEO
Project description:Gene and retrotransposon expression analysis for WT, Pld6 KO, and Dnmt3l KO male germ cells during spermatogenesis
| PRJNA289871 | ENA
Project description:DNA methylation analysis for mouse spermatogonia defficient in Pld6.
| PRJNA1258301 | ENA
Project description:Retrotransposon expression analysis for mouse spermatogonia defficient in Dnmt3l and Pld6.
| PRJNA1258307 | ENA
Project description:Gene and retrotransposon expression analysis in the F1 hybrid background of B6 and MSM for WT, Pld6 KO, and Dnmt3l KO male germ cells
| PRJNA314334 | ENA
Project description:Defective germline reprogramming in Miwi2- and Dnmt3l-deficient mice results in the failure to reestablish transposon silencing, meiotic arrest and progressive loss of spermatogonia. Here we sought to understand the molecular basis for this spermatogonial dysfunction. Through a combination of imaging, conditional genetics and transcriptome analysis, we demonstrate that germ cell elimination in the respective mutants arises due to defective germline reprogramming rather than a function for the respective factors within spermatogonia. In both Miwi2-/- and Dnmt3l-/- spermatogonia the intracisternal-A particle (IAP) family of endogenous retroviruses is de-repressed, but in contrast to meiotic cells DNA damage is not observed. Instead we find that unmethylated IAP promoters rewire the spermatogonial transcriptome by driving expression of neighboring host genes. In summary, defective reprogramming deregulates the spermatogonial transcriptome that may underlie spermatogonial dysfunction.
2018-03-09 | E-MTAB-6202 | biostudies-arrayexpress