Ontology highlight
ABSTRACT:
PROVIDER: PRJNA278140 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1914880.fastq.gz | Fastqsanger.gz | |||
| SRR1914890_1.fastq.gz | Fastqsanger.gz | |||
| SRR1914890_2.fastq.gz | Fastqsanger.gz | |||
| SRR1914881.fastq.gz | Fastqsanger.gz | |||
| SRR1914891_1.fastq.gz | Fastqsanger.gz |
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Project description:The postnatal neurodevelopmental disorder Rett syndrome (RTT) is caused by mutations in the gene encoding Methyl-CpG-binding Protein 2 (MeCP2). Despite decades of research, it remains unclear how MeCP2 actually regulates transcription or why RTT features appear only 6-18 months after birth. We examined MeCP2 binding to methylated cytosine in the CH context (mCH, where H = A, C, or T) in the adult mouse brain and found that MeCP2 binds these mCH sites, influencing nucleosome positioning and transcription. Strikingly, this pattern is unique to the mature nervous system, as it requires the increase in mCH after birth to reveal differences in MeCP2 binding to mCG, mCH, and non-methylated DNA elements. This study provides insight into the molecular mechanism governing MeCP2 targeting and how this targeting might contribute to the delayed onset of RTT symptoms. MeCP2 ChIP-Seq were conducted from ~ 7-week-old hypothalamus tissues from Mecp2-/y; MECP2-EGFP mice.
2015-04-15 | E-GEOD-66868 | biostudies-arrayexpress
Project description:The postnatal neurodevelopmental disorder Rett syndrome (RTT) is caused by mutations in the gene encoding Methyl-CpG-binding Protein 2 (MeCP2). Despite decades of research, it remains unclear how MeCP2 actually regulates transcription or why RTT features appear only 6-18 months after birth. We examined MeCP2 binding to methylated cytosine in the CH context (mCH, where H = A, C, or T) in the adult mouse brain and found that MeCP2 binds these mCH sites, influencing nucleosome positioning and transcription. Strikingly, this pattern is unique to the mature nervous system, as it requires the increase in mCH after birth to reveal differences in MeCP2 binding to mCG, mCH, and non-methylated DNA elements. This study provides insight into the molecular mechanism governing MeCP2 targeting and how this targeting might contribute to the delayed onset of RTT symptoms. Mnase-Seq were conducted from 7-week-old hypothalamus from MeCP2 knockout mice and their age and genetic background matched wild types control mice.
2015-04-15 | E-GEOD-66869 | biostudies-arrayexpress
Project description:MeCP2 binds to mCH as neurons mature, influencing transcription and onset of Rett syndrome [Mnase-Seq]
| PRJNA278145 | ENA
Project description:MeCP2 binds to mCH as neurons mature, influencing transcription and onset of Rett syndrome [mRNA-Seq]
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Project description:MeCP2 binds to mCH as neurons mature, influencing transcription and onset of Rett syndrome [ChIP-Seq]
| PRJNA278146 | ENA
Project description:The postnatal neurodevelopmental disorder Rett syndrome (RTT) is caused by mutations in the gene encoding Methyl-CpG-binding Protein 2 (MeCP2). Despite decades of research, it remains unclear how MeCP2 actually regulates transcription or why RTT features appear only 6-18 months after birth. We examined MeCP2 binding to methylated cytosine in the CH context (mCH, where H = A, C, or T) in the adult mouse brain and found that MeCP2 binds these mCH sites, influencing nucleosome positioning and transcription. Strikingly, this pattern is unique to the mature nervous system, as it requires the increase in mCH after birth to reveal differences in MeCP2 binding to mCG, mCH, and non-methylated DNA elements. This study provides insight into the molecular mechanism governing MeCP2 targeting and how this targeting might contribute to the delayed onset of RTT symptoms. mRNA-Seq were conducted from 7-week-old hypothalamus from MeCP2 knockout mice and their age and genetic background matched wild types control mice. Additonal mRNA-Seq were conducted from 7-week-old hypothalamus from MeCP2 transgenic mice and their age and genetic background matched wild types control mice.
2015-04-15 | E-GEOD-66870 | biostudies-arrayexpress
Project description:The postnatal neurodevelopmental disorder Rett syndrome (RTT) is caused by mutations in the gene encoding Methyl-CpG-binding Protein 2 (MeCP2). Despite decades of research, it remains unclear how MeCP2 actually regulates transcription or why RTT features appear only 6-18 months after birth. We examined MeCP2 binding to methylated cytosine in the CH context (mCH, where H = A, C, or T) in the adult mouse brain and found that MeCP2 binds these mCH sites, influencing nucleosome positioning and transcription. Strikingly, this pattern is unique to the mature nervous system, as it requires the increase in mCH after birth to reveal differences in MeCP2 binding to mCG, mCH, and non-methylated DNA elements. This study provides insight into the molecular mechanism governing MeCP2 targeting and how this targeting might contribute to the delayed onset of RTT symptoms.
2015-04-15 | GSE66869 | GEO
Project description:The postnatal neurodevelopmental disorder Rett syndrome (RTT) is caused by mutations in the gene encoding Methyl-CpG-binding Protein 2 (MeCP2). Despite decades of research, it remains unclear how MeCP2 actually regulates transcription or why RTT features appear only 6-18 months after birth. We examined MeCP2 binding to methylated cytosine in the CH context (mCH, where H = A, C, or T) in the adult mouse brain and found that MeCP2 binds these mCH sites, influencing nucleosome positioning and transcription. Strikingly, this pattern is unique to the mature nervous system, as it requires the increase in mCH after birth to reveal differences in MeCP2 binding to mCG, mCH, and non-methylated DNA elements. This study provides insight into the molecular mechanism governing MeCP2 targeting and how this targeting might contribute to the delayed onset of RTT symptoms.
2015-04-15 | GSE66868 | GEO
Project description:The postnatal neurodevelopmental disorder Rett syndrome (RTT) is caused by mutations in the gene encoding Methyl-CpG-binding Protein 2 (MeCP2). Despite decades of research, it remains unclear how MeCP2 actually regulates transcription or why RTT features appear only 6-18 months after birth. We examined MeCP2 binding to methylated cytosine in the CH context (mCH, where H = A, C, or T) in the adult mouse brain and found that MeCP2 binds these mCH sites, influencing nucleosome positioning and transcription. Strikingly, this pattern is unique to the mature nervous system, as it requires the increase in mCH after birth to reveal differences in MeCP2 binding to mCG, mCH, and non-methylated DNA elements. This study provides insight into the molecular mechanism governing MeCP2 targeting and how this targeting might contribute to the delayed onset of RTT symptoms.
2015-04-15 | GSE66870 | GEO
Project description:Mutations in the MECP2 gene cause the profound neurological disorder Rett syndrome. MeCP2 protein is an epigenetic reader that recruits the NCOR1/2 corepressor complexes to methylated cytosine in its canonical CG setting, but also to methylated CA motifs, which are abundant in neurons but rare in other cell types. In this study we set out to test the biological significance of this non-canonical mode of DNA binding. To achieve this, we replaced the endogenous MeCP2 DNA binding domain with that of MBD2, which only binds mCG. Knock-in mice expressing the hybrid “MM2” protein created by this domain-swap displayed severe Rett syndrome-like phenotypes. This indicates that binding to mCA, specifically the mCAC trinucleotide, is critical for normal brain function and it offers a plausible explanation for the delayed onset of Rett syndrome, due to the coincident late accumulation of mCAC and its cognate interpreter, MeCP2. We show that the small subset of genes aberrantly expressed in both Mecp2-null and MM2 mice is strikingly enriched for genes implicated in neurological disorders, highlighting targets with potential relevance to the Rett syndrome phenotype
2021-02-07 | GSE151859 | GEO