Integrated single cell analysis of chromatin accessibility and cell surface markers
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ABSTRACT:
PROVIDER: PRJNA685561 | ENA |
REPOSITORIES: ENA
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Project description:This SuperSeries is composed of the following subset Series:; GSE6942: Transcriptional profiling of bipotential embryonic liver cells to identify liver progenitor cell surface markers (moe430a). GSE6957: Transcriptional profiling of bipotential embryonic liver cells to identify liver progenitor cell surface markers (mouse4302). Experiment Overall Design: Refer to individual Series
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2017-05-23 | GSE99139 | GEO
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Project description:We carried out 10X sequencing of D27 induced pluripotent stem cell-derived megakaryocyte population which had been sorted for surface markers of megakaryocyte progenitors.
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Project description:We carried out 10X sequencing of D27 induced pluripotent stem cell-derived megakaryocyte population which had been sorted for surface markers of megakaryocyte progenitors.
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Project description:In vitro differentiation of human pluripotent stem cells into functional retinal pigment epithelial (RPE) cells for cell based reparative therapy of age-related macular degeneration (AMD). In the present study, we identify CD140b, CD56, GD2 and CD184 as central cell surface markers to evaluate hPSC-RPE differentiation efficiency, as well as a potential tool for the enrichment of hPSC-RPE during and after differentiation. Using these markers together with single cell RNA sequencing to evaluate the differentiation process, we have established an efficient xeno-free and defined monolayer differentiation methodology where culture on supportive human recombinant laminin eliminates the need for manual selection, allowing large-scale production of pure hPSC-RPE.
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Project description:Background: The cellular reservoir of latent HIV infection remains the main barrier to cure this virus. Elimination of this reservoir would be possible, if molecular identity of latently infected cells were fully elucidated. Biomarkers proposed previously were able to capture only a relatively small fraction of all reservoir cells. In the present study, we set out to conduct comprehensive molecular profiling, at the protein and RNA levels, of CD4+ T cells latently infected with HIV in vitro, using liquid chromatography-mass spectrometry (LC-MS) and RNA sequencing (RNA-Seq), respectively. Protein-based methods such as quantitative proteomic profiling using LC-MS may be more beneficial due to direct transferability of results to antibody-based approaches to capture latently infected cells. Integrated analysis of proteomic and transcriptomic data adds a level of validation and increases confidence in identified biomarkers. Flow cytometry and integrated HIV DNA assay were further used to enrich for latently infected cells with antibodies against selected biomarker proteins. Results: Using quantitative proteomics, we identified a total of 10,886 proteins (peptide level FDR < 0.05), of which 673 were up- and 780 down-regulated in latently infected compared to mock-infected cells in vitro (p < 0.05). Among these proteins, 21 were dysregulated at the RNA level in the same direction. Pathway analysis identified p53, mTOR, Wnt and NOTCH signaling, demonstrating that our in vitro model reflects known mechanisms of latency establishment and maintenance. Comparison of identified proteins with other proteomics studies revealed that identified molecular signatures of latency depend on technology and cell types used; however, a subset of proteins were identified both in the present, and at least one other study. Antibodies against selected protein markers, CEACAM1 and PLXNB2, could enrich for latently infected cells from mixed cell population 3-10 fold (5.8 fold average, p < 0.001). Conclusion: Two new molecules, CEACAM1 and PLXNB2, were identified as biomarkers for HIV latency. However, the level of enrichment for latently infected cells compared to biomarkers proposed previously was not improved. These results are consistent with the idea that each proposed biomarker defines only a subset of latently infected cells, and that a combined biomarker will be required to capture or target the latent HIV reservoir represented by different cell types.
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Project description:The high degree of genetic aberrations characteristic of high-grade serous ovarian cancer (HGSC) makes identification of the molecular features that drive tumor progression difficult. Here, we perform genome-wide RNAi screens and comprehensive expression analysis of cell surface markers in a panel of HGSC cell lines to identify genes that are critical to their survival. We report that the tetraspanin CD151 contributes to survival of a subset of HGSC cell lines associated with a ZEB transcriptional program and supports the growth of HGSC tumors. Moreover, we show that high CD151 expression is prognostic of poor clinical outcome. This study reveals cell-surface vulnerabilities associated with HGSC, provides a framework for identifying therapeutic targets, and reports a role for CD151 in HGSC.
2017-02-03 | GSE94304 | GEO
Project description:Purpose: Evaluate changes in chromatin accessibility between human embryonic stem cells and surface ectoderm cells with and without the transcription factor p63. Method: Chromatin accessibility profiles for human embryonic stem cells and surface ectoderm with and without p63 were generated by deep sequencing, in duplicate, with the Illumina NextSeq sequencer. Quality reads were assessed by fastq. Reads were aligned using Bowtie2, PCR duplicates and mitochondrial DNA were discarded, and peak calling was completed using MACS2. Non-reproducible peaks were filtered out by IDR with an FDR of 5%. Results: p63 fails to modify chromatin accessibility when ectopically expressed in human embryonic stem cells; differentiation of human embryonic stem cells to surface ectoderm results in the closure of some regions open in pluripotent cells and the opening of new regions; and loss of p63 in the surface ectoderm results in increased accessibility of 1/3 of the regions opened during surface ectoderm differentiation. Conclusion: p63's ability to modify chromatin accessibility is dependent upon the underlying epigenetic landscape, and when it can modify the landscape, it does so by closing regions that become open during ectoderm differentiation.
2018-11-06 | GSE119996 | GEO