Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA377642 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5307590_1.fastq.gz | Fastqsanger.gz | |||
| SRR5307590_2.fastq.gz | Fastqsanger.gz | |||
| SRR5307581_1.fastq.gz | Fastqsanger.gz | |||
| SRR5307581_2.fastq.gz | Fastqsanger.gz | |||
| SRR5307591_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 24 |
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Project description:In early embryos, DNA methylation is remodelled to initiate the developmental program. For mostly unknown reasons, methylation marks are acquired unequally between embryonic and placental cells. To better understand this, we generated high-resolution maps of DNA methylation in mouse mid-gestation (E10.5) embryo and placenta. We uncovered specific subtypes of differentially methylated regions (DMRs) that contribute directly to the developmental asymmetry existing between mid-gestation embryo and placenta. We show that the asymmetry between embryonic and placental DNA methylation patterns occurs rapidly during the acquisition of marks in the post-implanted conceptus (E3.5-E6.5), and that these patterns are long-lasting across subtypes of DMRs throughout prenatal development and in somatic tissues. We reveal that at the peri-implantation stages, the de novo methyltransferase activity of DNMT3B is the main driver of methylation marks on asymmetric DMRs, and that DNMT3B can largely compensate for lack of DNMT3A in the epiblast and extraembryonic ectoderm, whereas DNMT3A can only partially palliate for the absence of DNMT3B. However, as development progresses and as DNMT3A becomes the principal de novo methyltransferase, the compensatory DNA methylation mechanism on DMRs becomes less effective.
2020-02-18 | GSE95610 | GEO
Project description:One of the most important topic in mammalian embryogenesis is cell lineage segregation. Briefly, one totipotent zygote will develop into inner cell mass (ICM) and trophectoderm (TE) at blastocyst stage, then the ICM will finally develop into multiple somatic cell lineages and TE will majorly become the placenta tissue which supports and protects the development of the embryo proper. Multiple extrinsic and intrinsic regulatory pathways are involved in facilitating the appropriate development of the embryo. Epigenetic reprogramming is one of the most pervasive events during mouse embryo development(Li, 2002). Recent studies had implied that distinct features for the establishment of DNA methylation(Monk et al., 1987) and histone modifications especially H3K27me3(Liu et al., 2016) during mouse early embryo development. The re-establishment of DNA methylation in early mouse embryos starts at blastocyst stage (about embryonic day 3.5, E3.5) and peaks around the gastrulation stage, while the re-establishment of H3K27me3 exhibits a great level of dynamics and gradually increased CpG preference during pre-implantation embryo development(Liu et al., 2016). However, the underlying epigenetic mechanism concerning the lineage segregation and developmental competence restriction between the pluripotent embryo proper and the supporting extraembryonic tissues especially extraembryonic ectoderm (ExE) remains largely unknown. Surprisingly, no significant difference exists for the distribution of H3K27me3 and DNA methylation between ICM and TE in the preimplantation embryos. Therefore, it is of great importance for unveiling the interplays between H3K27me3 and DNA methylation involving in the restriction of developmental competence between embryonic cells and extraembryonic cells in post-implantation embryos.
2018-03-16 | GSE104243 | GEO
Project description:First lineage specification in the mammalian blastocyst embryo leads to formation of the inner cell mass (ICM) and trophectoderm (TE), which respectively give rise to the embryo proper and extraembryonic tissues. We show histone methylation asymmetry on promoters in the first two developmental lineages, and highlight epigenetic skewing associated with derivation of embryonic stem (ES) cells.
2010-02-10 | GSE17387 | GEO
Project description:Background Hemispheric asymmetry in neuronal processes is a fundamental feature of the human brain and drives symptom lateralization in Parkinson's disease (PD), but its molecular determinants are unknown. Here, we identify divergent epigenetic patterns involved in hemispheric asymmetry by profiling DNA methylation in isolated prefrontal cortex neurons from control and PD brain hemispheres. DNA methylation is fine-mapped at enhancers and promoters, genome-wide, by targeted bisulfite sequencing in two independent sample cohorts. Results We find that neurons of the human prefrontal cortex exhibit hemispheric differences in DNA methylation. Hemispheric asymmetry in neuronal DNA methylation patterns is largely mediated by differential CpH methylation, and chromatin conformation analysis finds that it targets thousands of genes. With aging, there is a loss of hemispheric asymmetry in neuronal epigenomes, such that hemispheres epigenetically converge in late life. In neurons of PD patients, hemispheric asymmetry in DNA methylation is greater than in controls and involves many PD risk genes. Epigenetic, transcriptomic, and proteomic differences between PD hemispheres correspond to the lateralization of PD symptoms, with abnormalities being most prevalent in the hemisphere matched to side of symptom predominance. Hemispheric asymmetry and symptom lateralization in PD is linked to genes affecting neurodevelopment, immune activation, and synaptic transmission. PD patients with a long disease course have greater hemispheric asymmetry in neuronal epigenomes than those with a short disease course. Conclusions Hemispheric differences in epigenetic gene regulation are prevalent in neurons and may affect the progression and symptoms of PD.
2020-02-12 | GSE135035 | GEO
Project description:Background Hemispheric asymmetry in neuronal processes is a fundamental feature of the human brain and drives symptom lateralization in Parkinson's disease (PD), but its molecular determinants are unknown. Here, we identify divergent epigenetic patterns involved in hemispheric asymmetry by profiling DNA methylation in isolated prefrontal cortex neurons from control and PD brain hemispheres. DNA methylation is fine-mapped at enhancers and promoters, genome-wide, by targeted bisulfite sequencing in two independent sample cohorts. Results We find that neurons of the human prefrontal cortex exhibit hemispheric differences in DNA methylation. Hemispheric asymmetry in neuronal DNA methylation patterns is largely mediated by differential CpH methylation, and chromatin conformation analysis finds that it targets thousands of genes. With aging, there is a loss of hemispheric asymmetry in neuronal epigenomes, such that hemispheres epigenetically converge in late life. In neurons of PD patients, hemispheric asymmetry in DNA methylation is greater than in controls and involves many PD risk genes. Epigenetic, transcriptomic, and proteomic differences between PD hemispheres correspond to the lateralization of PD symptoms, with abnormalities being most prevalent in the hemisphere matched to side of symptom predominance. Hemispheric asymmetry and symptom lateralization in PD is linked to genes affecting neurodevelopment, immune activation, and synaptic transmission. PD patients with a long disease course have greater hemispheric asymmetry in neuronal epigenomes than those with a short disease course. Conclusions Hemispheric differences in epigenetic gene regulation are prevalent in neurons and may affect the progression and symptoms of PD.
2020-02-12 | GSE145153 | GEO
Project description:Background Hemispheric asymmetry in neuronal processes is a fundamental feature of the human brain and drives symptom lateralization in Parkinson's disease (PD), but its molecular determinants are unknown. Here, we identify divergent epigenetic patterns involved in hemispheric asymmetry by profiling DNA methylation in isolated prefrontal cortex neurons from control and PD brain hemispheres. DNA methylation is fine-mapped at enhancers and promoters, genome-wide, by targeted bisulfite sequencing in two independent sample cohorts. Results We find that neurons of the human prefrontal cortex exhibit hemispheric differences in DNA methylation. Hemispheric asymmetry in neuronal DNA methylation patterns is largely mediated by differential CpH methylation, and chromatin conformation analysis finds that it targets thousands of genes. With aging, there is a loss of hemispheric asymmetry in neuronal epigenomes, such that hemispheres epigenetically converge in late life. In neurons of PD patients, hemispheric asymmetry in DNA methylation is greater than in controls and involves many PD risk genes. Epigenetic, transcriptomic, and proteomic differences between PD hemispheres correspond to the lateralization of PD symptoms, with abnormalities being most prevalent in the hemisphere matched to side of symptom predominance. Hemispheric asymmetry and symptom lateralization in PD is linked to genes affecting neurodevelopment, immune activation, and synaptic transmission. PD patients with a long disease course have greater hemispheric asymmetry in neuronal epigenomes than those with a short disease course. Conclusions Hemispheric differences in epigenetic gene regulation are prevalent in neurons and may affect the progression and symptoms of PD.
2020-02-12 | GSE135037 | GEO
Project description:Background Hemispheric asymmetry in neuronal processes is a fundamental feature of the human brain and drives symptom lateralization in Parkinson's disease (PD), but its molecular determinants are unknown. Here, we identify divergent epigenetic patterns involved in hemispheric asymmetry by profiling DNA methylation in isolated prefrontal cortex neurons from control and PD brain hemispheres. DNA methylation is fine-mapped at enhancers and promoters, genome-wide, by targeted bisulfite sequencing in two independent sample cohorts. Results We find that neurons of the human prefrontal cortex exhibit hemispheric differences in DNA methylation. Hemispheric asymmetry in neuronal DNA methylation patterns is largely mediated by differential CpH methylation, and chromatin conformation analysis finds that it targets thousands of genes. With aging, there is a loss of hemispheric asymmetry in neuronal epigenomes, such that hemispheres epigenetically converge in late life. In neurons of PD patients, hemispheric asymmetry in DNA methylation is greater than in controls and involves many PD risk genes. Epigenetic, transcriptomic, and proteomic differences between PD hemispheres correspond to the lateralization of PD symptoms, with abnormalities being most prevalent in the hemisphere matched to side of symptom predominance. Hemispheric asymmetry and symptom lateralization in PD is linked to genes affecting neurodevelopment, immune activation, and synaptic transmission. PD patients with a long disease course have greater hemispheric asymmetry in neuronal epigenomes than those with a short disease course. Conclusions Hemispheric differences in epigenetic gene regulation are prevalent in neurons and may affect the progression and symptoms of PD.
2020-02-12 | GSE135036 | GEO
Project description:The placental epigenome plays a vital role in regulating mammalian growth and development. Aberrations in placental DNA methylation are linked to several disease states, including intrauterine growth restriction and preeclampsia. Studying the evolution and development of the placental epigenome is critical to understanding the origin and progression of such diseases. Although high resolution studies have found substantial variation between placental methylomes of different species, the nature of methylome variation has yet to be characterized within any individual species. We conducted a study of placental DNA methylation at high resolution in multiple strains and closely related species of house mice (Mus musculus musculus, Mus m. domesticus, and M. spretus), across developmental timepoints (embryonic days 15 to 18), and between the labyrinthine transport and junctional endocrine layers. We observed substantial genome-wide methylation heterogeneity in mouse placenta compared to other differentiated tissues. Species-specific methylation profiles were concentrated in retrotransposon subfamilies, specifically RLTR10 and RLTR20 subfamilies. Regulatory regions such as gene promoters and CpG islands displayed cross-species conservation, but showed strong differences between layers and developmental timepoints. Partially methylated domains exist in the mouse placenta and widen during development. Taken together, our results characterize the mouse placental methylome as a highly heterogeneous and deregulated landscape globally, intermixed with actively regulated promoter and retrotransposon sequences.
2017-04-12 | GSE84350 | GEO
Project description:First lineage specification in the mammalian blastocyst embryo leads to formation of the inner cell mass (ICM) and trophectoderm (TE), which respectively give rise to the embryo proper and extraembryonic tissues. We show histone methylation asymmetry on promoters in the first two developmental lineages, and highlight epigenetic skewing associated with derivation of embryonic stem (ES) cells. Comparison of histone methylation patterns on promoters in the ICM, TE and in ES cells derived from ICM. ChIP-chip experiments using anti-H3K4me3 or anti-H3K27me3 antibodies. Two or three replicates per sample.
2010-05-14 | E-GEOD-17387 | biostudies-arrayexpress
Project description:Hemispheric asymmetry in neuronal processes is a fundamental feature of the human brain and drives symptom lateralization in Parkinson's disease (PD), but its molecular determinants are unknown. Here, we determine epigenetic changes and genes involved in hemispheric asymmetry in the healthy and PD brain. Neurons of healthy individuals exhibit numerous hemispheric differences in DNA methylation, affecting genes implicated in neurodegenerative diseases. In PD patients, hemispheric asymmetry in DNA methylation is even greater and involves many PD risk genes. Moreover, the lateralization of clinical PD symptoms involves epigenetic, transcriptional, and proteomic differences across hemispheres that affect neurodevelopment, immune activation, and synaptic transmission. In aging, healthy neurons demonstrate a progressive loss of hemisphere asymmetry in epigenomes that is amplified in PD. For PD patients, a long disease course is associated with retaining more hemispheric asymmetry in neuronal epigenomes. Hemispheric differences in epigenetic gene regulation are prevalent in neurons and may affect the progression and symptoms of PD.
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