Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA157029 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR944118_1.fastq.gz | Fastqsanger.gz | |||
| SRR944118_2.fastq.gz | Fastqsanger.gz | |||
| SRR944119_1.fastq.gz | Fastqsanger.gz | |||
| SRR944119_2.fastq.gz | Fastqsanger.gz | |||
| SRR944120_1.fastq.gz | Fastqsanger.gz |
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Project description:Binding of Polycomb repressive complex 2 (PRC2) and chromatin composition of the inactive X (Xi) before, during and after X chromosome inactivation reveal that spreading is driven by a combination of Xi-specific strong and moderate Ezh2 sites. Sequence context of these sites shows a moderate enrichment of SINEs and simple repeats. The general pattern of Ezh2 and H3K27me3 distribution over the chromosome reflect a graded concentration originating from strong Ezh2 sites, around which moderate sites are clustered, suggesting a hierarchy of Ezh2 sites govern spreading.
2012-11-01 | GSE36905 | GEO
Project description:Binding of Polycomb repressive complex 2 (PRC2) and chromatin composition of the inactive X (Xi) before, during and after X chromosome inactivation reveal that spreading is driven by a combination of Xi-specific strong and moderate Ezh2 sites. Sequence context of these sites shows a moderate enrichment of SINEs and simple repeats. The general pattern of Ezh2 and H3K27me3 distribution over the chromosome reflect a graded concentration originating from strong Ezh2 sites, around which moderate sites are clustered, suggesting a hierarchy of Ezh2 sites govern spreading. ChIP-seq of Ezh2 and H3K27me3 as well as the three active marks H3K4me3, H3K36me3 and RNA-POLII-serine5 phosphorylation (RNA-polII-S5P) in female cell lines: undifferentiated embryonic stem (ES) cells (d0), differentiating ES cells (d7) and a transformed embryonic fibroblast cell line (MEF).
2012-11-01 | E-GEOD-36905 | biostudies-arrayexpress
Project description:RNA-interference (RNAi) refers to a growing class of gene silencing phenomena defined by a requirement for small RNAs of 20-32 nt and the action of the Argonaute (Ago) family of ribonucleases. We have previously identified developmentally regulated small RNAs, using Northern blot analysis, that are expressed during X-chromosome inactivation in differentiating female mouse ES cels. We sought to identify these small RNAs using deep sequencing. We identified small RNAs that align to retrotransposon sequences and are enriched on the X-chromosome. LINE elements have been proposed to act as way stations during X-inactivation for the spreading of silencing along the entire chromosome, and our findings suggest that LINE elements found on the X-chromosome may be enriched for small RNAs relative to the genome. These results suggest that RNAi pathways are involved in regulating LINE elements during X-inactivation and ES cell differentiation.
2013-05-18 | GSE21888 | GEO
Project description:RNA-interference (RNAi) refers to a growing class of gene silencing phenomena defined by a requirement for small RNAs of 20-32 nt and the action of the Argonaute (Ago) family of ribonucleases. We have previously identified developmentally regulated small RNAs, using Northern blot analysis, that are expressed during X-chromosome inactivation in differentiating female mouse ES cels. We sought to identify these small RNAs using deep sequencing. We identified small RNAs that align to retrotransposon sequences and are enriched on the X-chromosome. LINE elements have been proposed to act as way stations during X-inactivation for the spreading of silencing along the entire chromosome, and our findings suggest that LINE elements found on the X-chromosome may be enriched for small RNAs relative to the genome. These results suggest that RNAi pathways are involved in regulating LINE elements during X-inactivation and ES cell differentiation. We size-fractionated total RNA from differentiating female mouse ES cells (day 4) into 18-24 nt and 25-45 nt populations and sequenced each fraction separately using the 454 platform. We used a karyotypically stable 40XX female ES cell line (EL16.7) with one X each of 129 and M. castaneus origins: 129 x (M.castaneus x 129).
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Project description:During X-inactivation, Xist RNA spreads along an entire chromosome to establish silencing. However, the mechanism and functional RNA elements involved in spreading remain undefined. By performing a comprehensive endogenous Xist deletion screen, we identify Repeat B as crucial for spreading Xist and maintaining Polycomb repressive complexes 1 and 2 (PRC1/PRC2) along the inactive X (Xi). Unexpectedly, spreading of these three factors is inextricably linked. Deleting Repeat B or its direct binding partner, HNRNPK, compromises recruitment of PRC1 and PRC2. In turn, ablating PRC1 or PRC2 impairs Xist spreading. Therefore, Xist and Polycomb complexes require each other to propagate along the Xi, suggesting a positive feedback mechanism between RNA initiator and protein effectors. Perturbing Xist/Polycomb spreading causes failure of de novo Xi silencing, with partial compensatory downregulation of the active X, and also disrupts topological Xi reconfiguration. Thus, Repeat B is a multifunctional element that integrates interdependent Xist/ Polycomb spreading, silencing, and changes in chromosome architecture.
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Project description:Translational research is commonly performed in the C57B6/J mouse strain, chosen for its genetic homogeneity and phenotypic uniformity. Here, we evaluate the suitability of the white-footed deer mouse (Peromyscus leucopus) as a model organism for aging research, offering a comparative analysis against C57B6/J and diversity outbred (DO) Mus musculus strains. Our study includes comparisons of body composition, skeletal muscle function, and cardiovascular parameters, shedding light on potential applications and limitations of P. leucopus in aging studies. Notably, P. leucopus exhibits distinct body composition characteristics, emphasizing reduced muscle force exertion and a unique metabolism, particularly in fat mass. Cardiovascular assessments showed changes in arterial stiffness, challenging conventional assumptions and highlighting the need for a nuanced interpretation of aging-related phenotypes. Our study also highlights inherent challenges associated with maintaining and phenotyping P. leucopus cohorts. Behavioral considerations, including anxiety-induced responses during handling and phenotyping assessment, pose obstacles in acquiring meaningful data. Moreover, the unique anatomy of P. leucopus necessitates careful adaptation of protocols designed for Mus musculus. While showcasing potential benefits, further extensive analyses across broader age ranges and larger cohorts are necessary to establish the reliability of P. leucopus as a robust and translatable model for aging studies.
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Project description:During development, changes in gene transcription are accompanied by changes in chromatin modification but the order and causality of events often remain unclear. Here we address this question using X-chromosome inactivation (XCI), which entails chromosome-wide gene silencing and heterochromatin formation. We initiate XCI in female, mouse embryonic stem cells by inducing Xist expression and monitor subsequent changes in transcription and chromatin modification by allele-specific TTseq and ChIPseq respectively. An unprecedented temporal resolution has enabled us to define early alterations in chromatin that are induced upon Xist RNA coating. Xist-induced repression begins with histone deacetylation, which involves the histone deacetylase HDAC3 and occurs before efficient loss of H3K4me3 and H3K4me1 modifications. Polycomb-associated repressive histone marks accumulate rapidly, starting with PRC1-associated H2AK119Ub and followed by PRC2-associated H3K27me3. However, polycomb accumulates initially at large premarked domains, some of which correspond to Xist entry sites, and then spreads into genes. We also show that spreading can only ensue when transcriptional silencing has occurred. These results establish a detailed epigenomic time course for XCI and reveal a hierarchy of events with chromatin playing an important role in transcriptional silencing of the X chromosome.
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