The effect of the Pld6 and Dnmt3l mutations on DNA methylation and expression of retrotransposons in mouse male germ cells
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ABSTRACT:
PROVIDER: PRJNA289866 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2102030.fastq.gz | Fastqsanger.gz | |||
| SRR2102040_1.fastq.gz | Fastqsanger.gz | |||
| SRR2102040_2.fastq.gz | Fastqsanger.gz | |||
| SRR2102050.fastq.gz | Fastqsanger.gz | |||
| SRR2102031.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.
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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.
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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.
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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.
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Project description:Retrotransposon expression analysis for mouse spermatogonia defficient in Dnmt3l and Pld6.
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Project description:DNA methyltransferase 3A (DNMT3A) and DNA methyltransferase 3-Like (DNMT3L) form functional heterotetramers and ATRX-DNMT3-DNMT3L (ADD) domains, shared by both DNMT3A and DNMT3L, recognizes histone H3 tail unmethylated at lysine-4 (H3K4me0) to deposit DNA methylation properly in mammalian germ cells. However, the combinational and differential role of ADD domains of DNMT3A and DNMT3L in vivo has not been fully defined. Here we analyze both female and male germ cells derived from mouse with amino-acid substitutions in ADD domains of DNMT3A and/or DNMT3L that impair their domain function. Loss of either DNMT3A-ADD or DNMT3L-ADD domain function shows moderate reduction of global CG methylation level, but in different degree, in both germ cells. However, when both DNMT3A and DNMT3L lost their ADD domain functions, reduction of the global CG methylation level is much more severe and comparable with that of Dnmt3a/3L knockout germ cells. In contrast, such double mutant germ cells have thousands of genomic regions where non-CG methylation is aberrantly accumulated. These results highlight a critical role of the combinational function of ADD domains for the robust CG and non-CG methylation in germ cells.
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Project description:DNA methyltransferase 3A (DNMT3A) and DNA methyltransferase 3-Like (DNMT3L) form functional heterotetramers and ATRX-DNMT3-DNMT3L (ADD) domains, shared by both DNMT3A and DNMT3L, recognizes histone H3 tail unmethylated at lysine-4 (H3K4me0) to deposit DNA methylation properly in mammalian germ cells. However, the combinational and differential role of ADD domains of DNMT3A and DNMT3L in vivo has not been fully defined. Here we analyze both female and male germ cells derived from mouse with amino-acid substitutions in ADD domains of DNMT3A and/or DNMT3L that impair their domain function. Loss of either DNMT3A-ADD or DNMT3L-ADD domain function shows moderate reduction of global CG methylation level, but in different degree, in both germ cells. However, when both DNMT3A and DNMT3L lost their ADD domain functions, reduction of the global CG methylation level is much more severe and comparable with that of Dnmt3a/3L knockout germ cells. In contrast, such double mutant germ cells have thousands of genomic regions where non-CG methylation is aberrantly accumulated. These results highlight a critical role of the combinational function of ADD domains for the robust CG and non-CG methylation in germ cells.
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