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An abundance of binary promoter switches in lineage-determining transcription factors indicates a digital component of cell fate determination

ABSTRACT: An abundance of binary promoter switches in lineage-determining transcription factors indicates a digital component of cell fate determination

PROVIDER: PRJNA1011326 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25863313_1.fastq.gz	Fastqsanger.gz
	SRR25863313_2.fastq.gz	Fastqsanger.gz
	SRR25863314_1.fastq.gz	Fastqsanger.gz
	SRR25863314_2.fastq.gz	Fastqsanger.gz
	SRR25863315_1.fastq.gz	Fastqsanger.gz

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An abundance of binary promoter switches in lineage-determining transcription factors indicates a digital component of cell fate determination

Project description:An examination of transcription factor genes revealed an abundance of convergent and divergent sense/antisense promoter pairs, suggesting that competing promoters may control cell fate determination. We used 5' single cell RNAseq (5' scRNAseq) to examine divergent and convergent transcription in CD34+ hematopoietic progenitors, freshly purified innate lymphocytes from tonisl, and peripheral blood NK cells

2023-10-27 | GSE242100 | GEO

Abundant binary promoter switches in lineage-determining transcription factors indicate a digital component of cell fate determination.

Project description:Previous studies of the murine Ly49 and human KIR gene clusters implicated competing sense and antisense promoters in the control of variegated gene expression. In the current study, an examination of transcription factor genes defines an abundance of convergent and divergent sense/antisense promoter pairs, suggesting that competing promoters may control cell fate determination. Differentiation of CD34+ hematopoietic progenitors in vitro shows that cells with GATA1 antisense transcription have enhanced GATA2 transcription and a mast cell phenotype, whereas cells with GATA2 antisense transcription have increased GATA1 transcripts and an erythroblast phenotype. Detailed analyses of the AHR and RORC genes demonstrate the ability of competing promoters to act as binary switches and the association of antisense transcription with an immature/progenitor cell phenotype. These data indicate that alternative cell fates generated by promoter competition in lineage-determining transcription factors contribute to the programming of cell differentiation.

| S-EPMC10842785 | biostudies-literature

Cell Fate Determining Molecular Switches and Signaling Pathway in Pax7-expressing Somitic Mesoderm

Project description:During development, different cell types are originated from a common progenitor at a specific time frame. Previous lineage tracing of Pax7+ progenitors in somitic mesoderm has built the foundation of its development trajectory towards dermis, brown adipocytes, and skeletal muscle at dorsal trunk. Yet the molecular switches and mechanisms of such differentiation remain unknown. By combining inducible lineage tracing and single-cell RNA sequencing, here we show the transcriptomic profile of the Pax7 lineage, precise differentiation time point, and transcription factors that could drive lineage-specific differentiation. Utilizing surface markers identified in each cell types, we successfully enriched brown adipocytes, dermal fibroblasts, and cell-type specific progenitors for in vitro culture. Further characterization has shown the importance of Wnt5a and Rgcc for lineage development during embryogenesis. We also propose eFAP (embryonic fibro/adipogenic progenitor) that resembles adult FAPs lineage potentials. The work provides further understanding of the Pax7 lineage during embryonic development.

2022-04-12 | GSE158887 | GEO

Determining cell type abundance and expression from bulk tissues with digital cytometry.

Project description:Single-cell RNA-sequencing has emerged as a powerful technique for characterizing cellular heterogeneity, but it is currently impractical on large sample cohorts and cannot be applied to fixed specimens collected as part of routine clinical care. We previously developed an approach for digital cytometry, called CIBERSORT, that enables estimation of cell type abundances from bulk tissue transcriptomes. We now introduce CIBERSORTx, a machine learning method that extends this framework to infer cell-type-specific gene expression profiles without physical cell isolation. By minimizing platform-specific variation, CIBERSORTx also allows the use of single-cell RNA-sequencing data for large-scale tissue dissection. We evaluated the utility of CIBERSORTx in multiple tumor types, including melanoma, where single-cell reference profiles were used to dissect bulk clinical specimens, revealing cell-type-specific phenotypic states linked to distinct driver mutations and response to immune checkpoint blockade. We anticipate that digital cytometry will augment single-cell profiling efforts, enabling cost-effective, high-throughput tissue characterization without the need for antibodies, disaggregation or viable cells.

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Cell Fate Determining Molecular Switches and Signaling Pathway in Pax7-expressing Somitic Mesoderm

Project description:Cell Fate Determining Molecular Switches and Signaling Pathway in Pax7-expressing Somitic Mesoderm

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YAP and TAZ Dictate Binary Pan-Cancer Superclasses

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YAP and TAZ Dictate Binary Pan-Cancer Superclasses

Project description:This SuperSeries is composed of the SubSeries listed below. We defined pan-cancer binary classes based on distinct expression of YAP (and its paralog TAZ/ WWTR1) and YAP-responsive adhesion regulators. Combining informatics with in vivo and in vitro gain- and loss-of-function studies across multiple murine and human tumor types, we showed that opposite pro- or anti-cancer YAP activity functionally defines binary YAPon or YAPoff cancer classes that express or silence YAP, respectively. Essentially all leukemia and lymphoma fall into the YAPoff class, as do multiple neural and neuroendocrine YAPoff solid cancers. YAPoff solid cancers are frequently RB1-/-, such as retinoblastoma, small cell lung cancer and neuroendocrine prostate cancer. YAP-silencing was intrinsic to the cell-of-origin, or acquired with lineage-switching and drug-resistance. The binary cancer groups exhibit distinct YAP-dependent adhesive behavior, and pharmaceutical vulnerabilities, underscoring clinical relevance. Mechanistically, whereas YAP induces cell cycle genes in YAPon cancers, extensive RNAseq data showed that forced YAP expression in YAPoff cancers instead activated adhesion genes that are normally co-silenced with YAP. YAP regulates both of these anti-cancer adhesive or pro-cancer cell cycle programs through the TEAD DNA binding family (TEAD1-4). YAP/TEAD targets AP1-bound enhancers in YAPon cancers, but Chipseq studies revealed that in YAPoff cancers, YAP/TEAD instead targeted elements co-bound with neural and neuroendocrine lineage-defining basic helix-loop-helix (bHLH) and Homeobox transcription factors (e.g. NEUROD, ASCL1, NKX2, OTX2). A CRISPR screen revealed that, among the adhesion regulators, ITGAV/ITGB5 pair are required for YAP induced cytostasis in YAPoff cancers. YAP is thus pivotal across all cancer, but in opposite pro- or anti-cancer ways, which define contrasting genetic and drug sensitivities.

2021-06-21 | GSE144975 | GEO

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