Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA383864 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5467232_1.fastq.gz | Fastqsanger.gz | |||
| SRR5467232_2.fastq.gz | Fastqsanger.gz | |||
| SRR5467233_1.fastq.gz | Fastqsanger.gz | |||
| SRR5467233_2.fastq.gz | Fastqsanger.gz | |||
| SRR5467234_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 6 |
Similar Datasets
Project description:Expression analysis of mouse embryonic stem cell (mESC) derived neuronal cell-types
| PRJNA138497 | ENA
Project description:Circular RNA has been reported to be dynamically expressed during embryonic development and regulates human embryonic stem cells (hESCs), but the identification and regulation of functional circular RNA in mouse embryonic stem cells (mESC) remains unclear. Here we found over 1,000 circular RNAs in different mESC states. One of these, circular RNA Kat6b-exon2 (circKat6b-e2), was significantly overexpressed in mESCs. Furthermore, short-hair RNA (shRNA) mediated knockdown of circKat6b-e2 expression significantly inhibited mESC self-renewal and EB differentiation. The transcriptome also revealed that circKat6b-e2 is required to ensure the differentiation of the mESC lineage. Finally, we also found that more Alu elements surrounding circKat6b-e2 were necessary factors for its expression. Conclusions: our study shows that Alu element-dependent expression of circKat6b-e2 mediates mESC self-renewal and lineage differentiation.
2022-08-28 | GSE211667 | GEO
Project description:We employed bulk RNA sequencing to interrogate the consequence of conditional BRD4 deletion in mouse embryonic stem cell (mESC)-derived cardiac progenitor cells.
2024-01-15 | GSE184919 | GEO
Project description:scRNA-seq of mouse embryonic stem cells (mESC) derived from four different genetic backgrounds grown in ground state conditions and differentiated towards an epiblast stem cell like (EpiSCL) population.
2020-12-15 | E-MTAB-8844 | biostudies-arrayexpress
Project description:Pluripotent stem cells can give rise to the three embryonic germ layers and the characterization of their properties is crucial to exploit their therapeutic potential. Mouse embryonic stem cells (mESCs) are isolated and usually maintained in vitro in a primed state that resembles the post-implantation epiblast features. Furthermore, primed mESCs can be de-differentiated to a naive state that resembles the pre-implantation inner cell mass (ICM). Cell differentiation or genotoxic stress, among others, can alter DNA replication, which is a flexible process able to adapt to different cellular contexts. Here, we demonstrate that primed-to-naive mESC reprogramming triggers replication fork slowdown, increased fork asymmetry and a compensatory activation of dormant origins. Using iPOND (“isolation of proteins on nascent DNA”) coupled to mass spectrometry we have characterized the changes in replisome composition between naive and primed mESCs. Several DNA repair factors, including MRE11 nuclease, are enriched in naive mESCs forks, while factors involved in ubiquitin-dependent protein metabolism are enriched in primed mESC forks. We report that primed-to-naive mESC de-differentiation promotes recruitment of MRE11 to the forks in response to transcription-replication conflicts, underlying the DNA replication rewiring required for efficient mESC reprogramming.
2024-04-03 | PXD041946 | Pride
Project description:mouse embryonic fibroblasts, embryonic stem cells, and induced pluripotent stem cells were compared via metabolomic analysis
2018-08-02 | MSV000082680 | GNPS
Project description:Empirical and anecdotal evidence have associated stress with accelerated hair greying (formation of unpigmented hairs), but the scientific evidence linking the two is scant. Here, we report that acute stress leads to hair greying through fast depletion of melanocyte stem cells (MeSCs). Combining adrenalectomy, denervation, chemogenetics, cell ablation, and MeSC-specific adrenergic receptor knockout, we found that stress-induced MeSC loss is independent of immune attack or adrenal stress hormones. Rather, hair greying results from activation of the sympathetic nerves that innervate the MeSC niche. Upon stress, sympathetic nerve activation leads to burst release of the neurotransmitter norepinephrine, which drives quiescent MeSCs into rapid proliferation, followed by differentiation, migration, and permanent depletion from the niche. Transient suppression of MeSC proliferation prevents stress-induced hair greying. Our studies demonstrate that acute stress-induced neuronal activity can drive rapid and permanent loss of somatic stem cells, and illustrate an example in which somatic stem cell maintenance is directly influenced by the overall physiological state of the organism.
2019-11-28 | GSE131566 | GEO
Project description:The inner cell mass of the mouse pre-implantation blastocyst is comprised of epiblast progenitor and primitive endoderm cells of which cognate embryonic (mESCs) or extra-embryonic (XEN) stem cell lines can be derived. Importantly, each stem cell type retains the defining properties and lineage restriction of their in vivo tissue of origin. Recently, we demonstrated that XEN-like cells arise within mESC cultures. This raises the possibility that mESCs can generate self-renewing XEN cells without the requirement for gene manipulation. We have developed a novel approach to convert mESCs to XEN cells (cXEN) using growth factors. We confirm that the down-regulation of the pluripotency transcription factor Nanog and the expression of primitive endoderm-associated genes Gata6, Gata4, Sox17 and Pdgfra are necessary for cXEN cell derivation. This approach highlights an important function for Fgf4 in cXEN cell derivation. Paracrine FGF-signalling compensates for the loss of endogenous Fgf4, which is necessary to exit mESC self-renewal, but not for XEN cell maintenance. Our cXEN protocol also reveals that distinct pluripotent stem cells respond uniquely to differentiation promoting signals. cXEN cells can be derived from mESCs cultured with Erk- and Gsk3-inhibitors (2i) and LIF, similarly to conventional mESCs. However, we find that epiblast stem cells (EpiSCs) derived from the post-implantation embryo are refractory to cXEN cell establishment, consistent with the hypothesis that EpiSCs represent a pluripotent state distinct from mESCs. In all, these findings suggest that the potential of mESCs includes the capacity to give rise to both extra-embryonic and embryonic lineages. A total of eight samples were analyzed. Three mouse embryonic stem cell (mESC) lines were used as a negative control, 2 embryo-derived extraembryonic endoderm (XEN) cell lines were used as a positive control, 3 converted XEN (cXEN) cells were used as the experiemental cell lines.
2012-06-04 | E-GEOD-38477 | biostudies-arrayexpress
Project description:Mouse embryonic stem cells (i.e., mESCs; line ESC 129-B13) were genetically modified using CRISPR-Cas9 to mutate the H3f3b locus, in order to carry homozygous lysine-to-alanine substitution of residues K9, K27 or K79. Two control mESC lines carrying knock-out of the H3f3a gene were used as background for the editing. Chromatin immunoprecipitation followed by sequencing (ChIP-seq) was performed to profile the changes in histone modifications, in the different H3.3 mutant mESC lines. The following histone modifications were profiled: H3K27ac (39685, Active Motif), H3K9ac (C5B11-9649, Cell Signalling Technology), H3K27me3 (C36B11, Cell Signalling Technology), H3K9me2 (D85B4, Cell Signalling Technology), H3K9me3 (D4W1U, Cell Signalling Technology). H3.3 (09-838, Merck-Millipore, purified polyclonal) ChIP-seq was performed in order to profile the deposition of this histone variant in the H3.3 K9A and K27A mESC mutant lines. SUZ12 (D39F6-3737, Cell Signalling Technology) ChIP-seq was performed to profile the genomic distribution of the Polycomb repressive complex 2 (i.e., PRC2). Two to three independent replicates per condition were grown and harvested for each ChIP experiment. Matched input controls were also generated in every experiment. Sequencing libraries were prepared using the NEBNext Ultra II library preparation kit (New England Biolabs) and sequenced on NextSeq500 or NextSeq2000 platforms in single-end mode.
2024-03-09 | E-MTAB-12868 | biostudies-arrayexpress
Project description:The epigenetic repressor BMI1 plays an integral role in promoting the self-renewal and proliferation of many adult stem cell populations, and also tumor types, primarily through silencing the Cdkn2a locus, which encodes the tumor suppressors p16Ink4a and p19Arf. However, in cutaneous melanoma, BMI1 drives epithelial-mesenchymal transition programs, and thus metastasis, while having little impact on proliferation or primary tumor growth. This raised questions about the requirement and role for BMI1 in melanocyte stem cell (MeSC) biology. Here, we demonstrate that murine melanocyte-specific Bmi1 deletion causes premature hair greying, which results from gradual MeSC loss. We establish that MeSC loss begins in the second hair cycle and is accompanied by melanocyte depletion. RNA-seq of MeSCs revealed that Bmi1 deletion induces transcriptional upregulation of p16Ink4a and p19Arf, mirroring the central role of BMI1 in other stem cell contexts. Additionally, the glutathione S-transferase enzymes Gsta1 and Gsta2 are downregulated by BMI1 loss, raising the possibility that MeSCs could be susceptible to oxidative stress. Accordingly, treatment with the antioxidant N-acetyl cysteine (NAC) partially rescued melanocyte expansion. Together, our data establish a critical role for BMI1 in MeSC maintenance that reflect a partial role for suppression of oxidative stress, and likely transcriptional repression of Cdkn2a.
2024-01-28 | GSE194373 | GEO