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: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:Gene and retrotransposon expression analysis for WT, Pld6 KO, and Dnmt3l KO male germ cells during spermatogenesis
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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
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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
Project description:Background: Down syndrome (DS) is characterized by a genome-wide profile of differential DNA methylation that is skewed towards hypermethylation in most tissues, including brain, and includes pan-tissue differential methylation. The molecular mechanisms involve the overexpression of genes related to DNA methylation on chromosome 21. Here, we stably overexpressed the chromosome 21 gene DNA methyltransferase 3L (DNMT3L) in the human SH-SY5Y neuroblastoma cell line and assayed DNA methylation at over 26 million CpGs by whole genome bisulfite sequencing (WGBS) at three different developmental phases (undifferentiated, differentiating, and differentiated). Results: DNMT3L overexpression resulted in global CpG and CpG island hypermethylation as well as thousands of differentially methylated regions (DMRs). The DNMT3L DMRs were skewed towards hypermethylation and mapped to genes involved in neurodevelopment, cellular signaling, and gene regulation. Consensus DNMT3L DMRs showed that cell lines clustered by genotype and then differentiation phase, demonstrating sets of common genes affected across neuronal differentiation. The hypermethylated DNMT3L DMRs from all pairwise comparisons were enriched for regions of bivalent chromatin marked by H3K4me3 as well as differentially methylated sites from previous DS studies of diverse tissues. In contrast, the hypomethylated DNMT3L DMRs from all pairwise comparisons displayed a tissue-specific profile enriched for regions of heterochromatin marked by H3K9me3 during embryonic development. Conclusions: Taken together, these results support a mechanism whereby regions of bivalent chromatin that lose H3K4me3 during neuronal differentiation are targeted by excess DNMT3L and become hypermethylated. Overall, these findings demonstrate that DNMT3L overexpression during neurodevelopment recreates a facet of the genome-wide DS DNA methylation signature by targeting known genes and gene clusters that display pan-tissue differential methylation in DS.
2021-03-05 | GSE168276 | GEO
Project description:DNA methyltransferase 3-like (DNMT3L), an epigenetic modulating factor known to participate in facilitating de novo DNA methylation with DNMT3A and DNMT3B, is mainly expressed in pluripotent stem cells and germ cells. We observed that Dnmt3l deficiency imped mesenchymal stem cells (MSCs) self-renewal and proliferation by colony forming unit – fibroblast (CFU-F) assay and growth curve test. Furthermore, calcium precipitation is dramatically decreased after 14 days of osteogenic induction in Dnmt3l KO mice derived MSCs. We further investigated the gene expression pattern in undifferentiated and day 3 of osteogenic induction MSCs derived from wild type and Dnmt3l KO mice respectively by RNA-sequencing, and found that differentially expressed genes (DEGs) before osteogenesis are highlighted in various pathways related to bone and the DEGs from day 3 of osteogenic induction MSCs are associated with proliferation and differentiation. Collectively, these results indicate that Dnmt3l deficiency abrogated MSCs property and may play role in MSC differentiation potential. By these results, we suggested that transiently expressed DNMT3L in pluripotent stem cells contribute to mediation of epigenetic mark establishment and have a lasting effect in mesenchymal stem cells.
2021-03-16 | GSE113844 | GEO
Project description:Loss of Tet1 expression causes global 5mC and 5hmC changes in stem and progenitor cells in mice and causes enhanced Pro-B cell self-renewal, increased DNA damage and B-lymphomageneis. In this study we performed reduced representative bisulfite sequencing (RRBS) of DNA from WT and Tet1 KO LSK cells. DNA methylation sequencing was performed and analyzed using an enhanced reduced representation (ERRBS) methodology as previously described. DNA was extracted from purified LSK cells of 6-month old WT and Tet1 KO mice, Bisulphite treatment was performed using the EZ DNA Methylation Kit (Zymo Research). Libraries were amplified according to illumina protocols and sequenced on an Illumina HiSeq2500 machine DNA methylation profiling of LSK cells in WT and Tet1 KO mice.
2015-04-12 | E-GEOD-65919 | biostudies-arrayexpress
Project description:The de novo DNA methyltransferase 3-like (Dnmt3L) is a catalytically inactive DNA methylase that has been previously shown to cooperate with Dnmt3a and Dnmt3b to methylate DNA. Dnmt3L is highly expressed in mouse embryonic stem cells (ESC) but its function in these cells is unknown. We here report that Dnmt3L is required for the differentiation of ESC into primordial germ cells (PGC) through activation of the homeotic gene Rhox5. By genome-wide analysis we found that Dnmt3L is a positive regulator of methylation at gene bodies of housekeeping genes and a negative regulator of methylation at promoters of bivalent genes. We demonstrate that Dnmt3L interacts with the Polycomb PRC2 complex in competition with the DNA methyltransferases Dnmt3a and Dnmt3b to maintain low the methylation level at H3H27me3 regions. Thus, in ESC, Dnmt3L counteracts the activity of de novo DNA methylases to keep low the level of DNA methylation at developmental gene promoters. Examination of Ezh2 ChIP-Seq in shGFP and shDnmt3L ESC. Examination of Dnmt3L ChIP-Seq in shGFP and shSuz12 ESC.
2013-09-27 | E-GEOD-49178 | biostudies-arrayexpress
Project description:The de novo DNA methyltransferase 3-like (Dnmt3L) is a catalytically inactive DNA methylase that has been previously shown to cooperate with Dnmt3a and Dnmt3b to methylate DNA. Dnmt3L is highly expressed in mouse embryonic stem cells (ESC) but its function in these cells is unknown. We here report that Dnmt3L is required for the differentiation of ESC into primordial germ cells (PGC) through activation of the homeotic gene Rhox5. By genome-wide analysis we found that Dnmt3L is a positive regulator of methylation at gene bodies of housekeeping genes and a negative regulator of methylation at promoters of bivalent genes. We demonstrate that Dnmt3L interacts with the Polycomb PRC2 complex in competition with the DNA methyl transferases Dnmt3a and Dnmt3b to maintain low the methylation level at H3H27me3 regions. Thus in ESC, Dnmt3L counteracts the activity of de novo DNA methylases to keep low the level of DNA methylation at developmental gene promoters. Examination of 5mC in shGFP and shDnmt3L ESC by MeDIP-Seq
2013-09-27 | E-GEOD-44642 | biostudies-arrayexpress