Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA289871 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2102040_1.fastq.gz | Fastqsanger.gz | |||
| SRR2102040_2.fastq.gz | Fastqsanger.gz | |||
| SRR2102031.fastq.gz | Fastqsanger.gz | |||
| SRR2102041_1.fastq.gz | Fastqsanger.gz | |||
| SRR2102041_2.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: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:Whole-genome DNA methylation analysis for purified WT, Pld6 KO, and Dnmt3l KO spermatogonia
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Project description:Small RNA sequencing analysis for male germ cells during spermatogenesis
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Project description:DNA methylatio of retrotransposon of male germ cells
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Project description:The RNA demethylase ALKBH5 is regarded as the “eraser” in N6-methyladenosine (m6A) modification. ALKBH5 deficiency has been reported to cause male infertility in mice; however, the mechanisms that confer disruption of spermatogenesis are not completely clear. In this study, we profiled testis samples from wild-type (WT) and Alkbh5 knockout (KO) mice by single-cell RNA sequencing (scRNA-seq). We obtained scRNA-seq data of 5596 and 6816 testis cells from a WT and KO mouse, respectively. Genetic profile differences between the groups were detected at different germ cell development stages, from the development of spermatogonia to sperm cells, as well as in macrophages, Sertoli cells, and Leydig cells. We further focused on differentially expressed genes related to spermatogenesis in germ cells and somatic cells (Sertoli cells and Leydig cells), and identified their functions and associated pathways by gene ontology enrichment analysis, such as chromatin-related functional pathways and Dnah8 gene, This study providing the first scRNA-seq profiles of the testes of ALKBH5-deficient mice highlights that ALKBH5 is an important transcription factor for germ cell development and spermatogenesis with new molecular mechanistic insight. These findings can provide the basis for further research into the causes and treatment of male infertility.
2021-12-09 | GSE190396 | GEO
Project description:We analyzed transcriptome profiles of postnatal germ cells and demonstrated that DNMT3L is important for spermatogonial stem/progenitor cell development Examination of wild-type and Dnmt3l knockout smaples in postnatal male germ cells
2014-07-03 | E-GEOD-54411 | biostudies-arrayexpress
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.
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Project description:While de novo DNA methylation (DNAme) in mammalian germ cells is dependent upon DNMT3A and DNMT3L, oocytes and spermatozoa show distinct patterns of DNAme. In mouse oocytes, de novo DNAme requires the lysine methyltransferase (KMTase) SETD2, which deposits H3K36me3. Surprisingly, we show here that SETD2 is dispensable for de novo DNAme in the male germline. Rather, the KMTase NSD1, which broadly deposits H3K36me2 in euchromatic regions, plays a critical role in de novo DNAme in prospermatogonia, including of imprinted genes. However, males deficient in germline NSD1 show a more severe defect in spermatogenesis than Dnmt3l-/- males. Furthermore, unlike DNMT3L, NSD1 safeguards a subset of genes against H3K27me3-associated transcriptional silencing. In contrast, H3K36me2 plays only a minor role in de novo DNAme during oogenesis and females with NSD1 deficient oocytes are fertile. Thus, the sexually dimorphic pattern of DNAme in mature mouse gametes is driven by distinct profiles of H3K36 methylation.
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Project description:In euakryotes, mRNAs must be exported from the nucleus to the cytsoplasm. NXF2 is highly expressed in the mouse male germ cells. We are interested in its function in spermatogenesis, espically in the nuclear RNA export in the testis. To this end, we made Nxf2 mutant mice by gene targeting. In an attempt to identify the mRNA substrates of NXF2, we perform the microarray experiments on testes. We used microarrays to check the expression profiles of the Nxf2 WT and KO 21d testes on C57BL/6 background. Experiment Overall Design: To examine the expression difference between WT and Nxf2 KO testes, we collected testes from juvenile mice of three ages ( 21d, 26d, 28d). Testis weight was similar between WT and KO mice at post-natal day 21. Three pairs of WT and KO 21d testes were chosen for microarray analysis.
2009-11-14 | E-GEOD-13526 | biostudies-arrayexpress