Aging alters the epigenetic asymmetry of HSC division [scRNA-Seq]
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ABSTRACT:
PROVIDER: PRJNA479965 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7477960_1.fastq.gz | Fastqsanger.gz | |||
| SRR7477960_2.fastq.gz | Fastqsanger.gz | |||
| SRR7477970_1.fastq.gz | Fastqsanger.gz | |||
| SRR7477970_2.fastq.gz | Fastqsanger.gz | |||
| SRR7477980_1.fastq.gz | Fastqsanger.gz |
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Project description:Aging alters the epigenetic asymmetry of HSC division
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Project description:Aging alters the epigenetic asymmetry of HSC division [scATAC-Seq]
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Project description:Hematopoietic stem cells (HSCs) balance self-renewal and differentiation to maintain homeostasis. With aging, the frequency of polar HSCs decreases. Cell polarity in HSCs is controlled by the activity of the small RhoGTPase Cdc42. Here we demonstrate, using a comprehensive set of paired daughter cell analyses that include single cell 3D-confocal imaging, single cell transplants, single cell RNA-seq as well as single cell ATAC-seq, that the outcome of HSC divisions is strongly linked to the polarity status before mitosis, which is in turn determined by the level of the activity Cdc42 in stem cells. Aged apolar HSCs undergo preferentially self-renewing symmetric divisions, resulting in daughter stem cells with reduced regenerative capacity and lymphoid potential, while young polar HSCs undergo preferentially asymmetric divisions. Mathematical modeling in combination with experimental data implies a mechanistic role of the asymmetric sorting of Cdc42 in determining the potential of daughter cells via epigenetic mechanisms. Therefore, molecules that control HSC polarity might serve as modulators of the mode of stem cell division regulating the potential of daughter cells.
2018-12-04 | GSE116708 | GEO
Project description:Hematopoietic stem cells (HSCs) balance self-renewal and differentiation to maintain homeostasis. With aging, the frequency of polar HSCs decreases. Cell polarity in HSCs is controlled by the activity of the small RhoGTPase Cdc42. Here we demonstrate, using a comprehensive set of paired daughter cell analyses that include single cell 3D-confocal imaging, single cell transplants, single cell RNA-seq as well as single cell ATAC-seq, that the outcome of HSC divisions is strongly linked to the polarity status before mitosis, which is in turn determined by the level of the activity Cdc42 in stem cells. Aged apolar HSCs undergo preferentially self-renewing symmetric divisions, resulting in daughter stem cells with reduced regenerative capacity and lymphoid potential, while young polar HSCs undergo preferentially asymmetric divisions. Mathematical modeling in combination with experimental data implies a mechanistic role of the asymmetric sorting of Cdc42 in determining the potential of daughter cells via epigenetic mechanisms. Therefore, molecules that control HSC polarity might serve as modulators of the mode of stem cell division regulating the potential of daughter cells.
2018-12-04 | GSE116707 | GEO
Project description:Hematopoietic stem cells (HSCs) balance self-renewal and differentiation to maintain homeostasis. With aging, the frequency of polar HSCs decreases. Cell polarity in HSCs is controlled by the activity of the small RhoGTPase cell division control protein 42 (Cdc42). Here we demonstrate-using a comprehensive set of paired daughter cell analyses that include single-cell 3D confocal imaging, single-cell transplants, single-cell RNA-seq, and single-cell transposase-accessible chromatin sequencing (ATAC-seq)-that the outcome of HSC divisions is strongly linked to the polarity status before mitosis, which is in turn determined by the level of the activity Cdc42 in stem cells. Aged apolar HSCs undergo preferentially self-renewing symmetric divisions, resulting in daughter stem cells with reduced regenerative capacity and lymphoid potential, while young polar HSCs undergo preferentially asymmetric divisions. Mathematical modeling in combination with experimental data implies a mechanistic role of the asymmetric sorting of Cdc42 in determining the potential of daughter cells via epigenetic mechanisms. Therefore, molecules that control HSC polarity might serve as modulators of the mode of stem cell division regulating the potential of daughter cells.
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Project description:We analyzed data from sequencing-based massively parallel reporter assays (MPRAs) retaining the strand orientation of the alignments. These analyses showed pervasive asymmetry in reporter signal from test element strand orientation. Present in elements derived from all regions of the human genome, we found test elements derived from gene bodies display concordant strand asymmetry with the sense orientation of the gene body. Furthermore, we observe that test elements form Alu sequence also present concordant strand asymmetry with Alu retrotransposon features. We establish sequence features that drive some of this asymmetry.
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Project description:Asymmetric selection of single-stranded guide RNAs from double-stranded RNA (dsRNA) precursors is crucial for RNA silencing-mediated gene regulation. However, the precise mechanisms for small RNA asymmetry remain unclear, especially since asymmetric selection can still occur under depletion of putative asymmetry sensors, Drosophila R2D2 and mammalian Dicer. Here we report direct contribution of mammalian Argonaute 2 (Ago2) to microRNA (miRNA) asymmetry. Ago2 selects strands with 5´-uridine/adenosine and thermodynamically unstable 5´-ends in parallel through its two sensor regions, which contact 5´-nucleobase and 5´-phosphate(s) of the prospective guide strands, respectively. Consistently, miRNA asymmetry shows characteristic digital-analog superposed patterns reflecting 5'-end nucleotide identity and thermodynamic stability. Furthermore, we demonstrate that cancer-associated miRNA variations reprogram asymmetric selection. Finally, our study presents a model of this universal principle that will aid a comprehensive understanding of miRNA function and therapeutic reinvention of RNA silencing in precision medicine. Immunoprecipitation of WT or mutant Ago2 in mouse ES cells (Ago-null background) and small RNA sequencing
2015-06-15 | E-GEOD-66022 | biostudies-arrayexpress