Demethylation and derepression of genomic retroelements in the skeletal muscles of aged mice
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ABSTRACT:
PROVIDER: PRJNA510380 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8330300_1.fastq.gz | Fastqsanger.gz | |||
| SRR8330300_2.fastq.gz | Fastqsanger.gz | |||
| SRR8330310_1.fastq.gz | Fastqsanger.gz | |||
| SRR8330310_2.fastq.gz | Fastqsanger.gz | |||
| SRR8330301_1.fastq.gz | Fastqsanger.gz |
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Project description:Changes in DNA methylation influence the aging process and contribute to aging phenotypes, but few studies have been conducted on DNA methylation changes in conjunction with skeletal muscle aging. We explored the DNA methylation changes in a variety of retroelement families throughout aging (at 2, 20, and 28 months of age) in murine skeletal muscles by methyl-binding domain sequencing (MBD-seq). The two following contrasting patterns were observed among the members of each repeat family in superaged mice: (1) hypermethylation in weakly methylated retroelement copies and (2) hypomethylation in copies with relatively stronger methylation levels, representing a pattern of “regression toward the mean” within a single retroelement family. Interestingly, these patterns depended on the sizes of the copies. While the majority of the elements showed a slight increase in methylation, the larger copies (>5 kb) displayed evident demethylation. All these changes were not observed in T cells. RNA sequencing revealed a global derepression of retroelements during the late phase of aging (between 20-28 months of age), which temporally coincided with retroelement demethylation. Following this methylation drift trend of “regression toward the mean”, aging tended to progressively lose the preexisting methylation differences and local patterns in the genomic regions that had been elaborately established during the early period of development.
2019-09-16 | GSE123954 | GEO
Project description:Changes in DNA methylation influence the aging process and contribute to aging phenotypes, but few studies have been conducted on DNA methylation changes in conjunction with skeletal muscle aging. We explored the DNA methylation changes in a variety of retroelement families throughout aging (at 2, 20, and 28 months of age) in murine skeletal muscles by methyl-binding domain sequencing (MBD-seq). The two following contrasting patterns were observed among the members of each repeat family in superaged mice: (a) hypermethylation in weakly methylated retroelement copies and (b) hypomethylation in copies with relatively stronger methylation levels, representing a pattern of "regression toward the mean" within a single retroelement family. Interestingly, these patterns depended on the sizes of the copies. While the majority of the elements showed a slight increase in methylation, the larger copies (>5 kb) displayed evident demethylation. All these changes were not observed in T cells. RNA sequencing revealed a global derepression of retroelements during the late phase of aging (between 20 and 28 months of age), which temporally coincided with retroelement demethylation. Following this methylation drift trend of "regression toward the mean," aging tended to progressively lose the preexisting methylation differences and local patterns in the genomic regions that had been elaborately established during the early period of development.
| S-EPMC6826136 | biostudies-literature
Project description:We aim at understanding how ionizing radiations (IR) increase the risk of developing myeloid leukemia. We recently showed that IR leads to the derepression of retroelements. We demonstrated that retroelements expression in aged HSCs is regulated by the heterochromatin repressive histone mark H3K9me3. However, the mechanisms by which IR specifically triggers retroelements expression in HSCs are unknown. We hypothesized that retroelements derepression is due to IR-induced heterochromatin changes. To answer this question, we performed H3K9me3 ChIP-seq experiments in hematopoietic stem cells sorted from mice one month after they were irradiated and compared them to controls hematopoietic stem cells sorted from non-irradiated mice.
2022-06-24 | E-MTAB-11865 | biostudies-arrayexpress
Project description:Skeletal muscle atrophy is one of the critical issues which elderly people face. The precise mechanism underlying muscle atrophy during aging is not fully understood. In order to identify miRNA whose expression is changed in age-associated muscle atrophy, we performed miRNA expression profiling of skeletal muscles in young and aged rats. Microarray analysis revealed differential miRNA expression in EDL and soleus muscles of aged rats compared with those of young rats. We next investigated whether the age-associated changes of miRNA expression observed in rats were recapitulated in mice and found that the expression level of miR-206 in EDL muscle and that of miR-196a in EDL and soleus muscles were respectively higher and lower in aged rodents than in young rodents. In mouse C2C12 myoblasts and myotubes, introduction of miR-196a decreased the protein level of Forkhead-box transcription factor Foxo1, a known target of miR-196a, indicating that miR-196a may regulate Foxo1 expression also in skeletal muscles. Furthermore, miR-196a overexpression exacerbated cell death caused by an exposure to hydrogen peroxide. Lastly, we demonstrated that expression of Foxo1 was elevated in EDL and soleus muscles of aged mice compared with those of young mice. These results suggest that miRNAs are involved in skeletal muscle atrophy during aging and that decreased miR-196a expression may protect skeletal muscle cells from oxidative stress in part through induction of Foxo1.
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Project description:We aim at understanding how ionizing radiations (IR) increase the risk of developing myeloid leukemia. We recently showed that IR leads to the derepression of retroelements. Retroelements are major contributors of gene regulatory networks. However, the impact of retroelements derepression on the HSC transcriptome and function remains to be addressed. We hypothesized that retroelements derepression is involved in HSC transcriptomic alterations. To answer this question, we performed RNA-seq experiments in hematopoietic stem cells sorted from mice one month after they were irradiated and compared them to controls hematopoietic stem cells sorted from non-irradiated mice.
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Project description:We generated a large transcriptome atlas of human skeletal muscles by collecting biopsies from 6 different muscles to determine molecular signatures that may be distinct between leg muscles. The biopsies were collected from gracilis (GR), semitendinosus (ST), vastus lateralis (VL), vastus medialis (VM), rectus femoris (RF), and gastrocnemius lateralis (GL) muscles. We also investigated molecular differences within the muscle by including two biopsies from the middle and distal sides of the semitendinosus muscle (STM and STD, respectively). In total, 128 samples from 20 individuals (aged 25 ± 3.6 yr) were analyzed.
| EGAS00001005904 | EGA
Project description:Genome-wide passive DNA demethylation in cleavage-stage mouse embryos is related to the cytoplasmic localization of the maintenance methyltransferase DNMT1. However, recent studies provided evidence of the nuclear localization of DNMT1 and its contribution to the maintenance of methylation levels of imprinted regions and other genomic loci in early embryos. Using the DNA-adenine methylase identification (DamID) method, we identified Dnmt1-binding regions in 4-cell and 8-cell embryos. The unbiased distribution of Dnmt1 peaks in the genic regions (promoters and CpG islands) as well as the absence of a correlation between the Dnmt1 peaks and the expression levels of the peak-associated genes refute the active participation of Dnmt1 in the transcriptional regulation of genes in the early developmental period. Instead, Dnmt1 was found to associate with genomic retroelements in a greatly biased fashion, particularly with the long interspersed nuclear elements (LINE1) and endogenous retrovirus type-K (ERVK) sequences. Transcriptomic analysis revealed that the transcripts of the Dnmt1-enriched retroelements were overrepresented in Dnmt1 knockdown embryos. Finally, methyl-CpG-binding-domain sequencing proved that the Dnmt1-enriched retroelements, which were densely methylated in wild-type embryos, became demethylated in the Dnmt1-depleted embryos. Our results indicate that Dnmt1 is involved in the repression of retroelements through DNA methylation in early mouse development.
2020-07-19 | GSE150462 | GEO
Project description:Genome-wide passive DNA demethylation in cleavage-stage mouse embryos is related to the cytoplasmic localization of the maintenance methyltransferase DNMT1. However, recent studies provided evidence of the nuclear localization of DNMT1 and its contribution to the maintenance of methylation levels of imprinted regions and other genomic loci in early embryos. Using the DNA-adenine methylase identification (DamID) method, we identified Dnmt1-binding regions in 4-cell and 8-cell embryos. The unbiased distribution of Dnmt1 peaks in the genic regions (promoters and CpG islands) as well as the absence of a correlation between the Dnmt1 peaks and the expression levels of the peak-associated genes refute the active participation of Dnmt1 in the transcriptional regulation of genes in the early developmental period. Instead, Dnmt1 was found to associate with genomic retroelements in a greatly biased fashion, particularly with the long interspersed nuclear elements (LINE1) and endogenous retrovirus type-K (ERVK) sequences. Transcriptomic analysis revealed that the transcripts of the Dnmt1-enriched retroelements were overrepresented in Dnmt1 knockdown embryos. Finally, methyl-CpG-binding-domain sequencing proved that the Dnmt1-enriched retroelements, which were densely methylated in wild-type embryos, became demethylated in the Dnmt1-depleted embryos. Our results indicate that Dnmt1 is involved in the repression of retroelements through DNA methylation in early mouse development.
2020-07-19 | GSE150463 | GEO