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Joint single-cell multiomic analysis identifies Aebp2 as a key regulator in Wnt3a induced asymmetric stem cell division

ABSTRACT: Joint single-cell multiomic analysis identifies Aebp2 as a key regulator in Wnt3a induced asymmetric stem cell division

PROVIDER: PRJNA713311 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13925000_1.fastq.gz	Fastqsanger.gz
	SRR13925000_2.fastq.gz	Fastqsanger.gz
	SRR13925001_1.fastq.gz	Fastqsanger.gz
	SRR13925001_2.fastq.gz	Fastqsanger.gz
	SRR13925002_1.fastq.gz	Fastqsanger.gz

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Joint single-cell multiomic analysis identifies Aebp2 as a key regulator in Wnt3a induced asymmetric stem cell division

Project description:Wnt signal usually functions as a spatial gradient. A localized Wnt3a can induce asymmetric division of mouse embryonic stem cells, whereas proximal daughter cells maintain self-renew and distal daughter cells acquire hallmarks of differentiation. Here, we develop an approach, SET-seq (same cell epigenome and transcriptome sequencing), to jointly profile epigenome and transcriptome in the same single cell. By utilizing SET-seq, we profile H3K27me3 and H3K4me3 with gene expression in Wnt3a induced asymmetric cell division. H3K27me3, but not H3K4me3, is correlatedly changed with gene expression. Single cells clustered by H3K27me3 recapitulate the clusters defined by gene expression. Furthermore, Aebp2, which is the regulator of H3K27me3, is important for the cell-fate decision with localized Wnt signal. Our results provide a convenient way to jointly profile epigenome and transcriptome in the same cell, and uncover the mechanistic insights into the gene regulatory programs for maintaining and resetting stem cell fate during differentiation.

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Joint single-cell multiomic analysis in Wnt3a induced asymmetric stem cell division.

Project description:Wnt signaling usually functions through a spatial gradient. Localized Wnt3a signaling can induce the asymmetric division of mouse embryonic stem cells, where proximal daughter cells maintain self-renewal and distal daughter cells acquire hallmarks of differentiation. Here, we develop an approach, same cell epigenome and transcriptome sequencing, to jointly profile the epigenome and transcriptome in the same single cell. Utilizing this method, we profiled H3K27me3 and H3K4me3 levels along with gene expression in mouse embryonic stem cells with localized Wnt3a signaling, revealing the cell type-specific maps of the epigenome and transcriptome in divided daughter cells. H3K27me3, but not H3K4me3, is correlated with gene expression changes during asymmetric cell division. Furthermore, cell clusters identified by H3K27me3 recapitulate the corresponding clusters defined by gene expression. Our study provides a convenient method to jointly profile the epigenome and transcriptome in the same cell and reveals mechanistic insights into the gene regulatory programs that maintain and reset stem cell fate during differentiation.

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Gene expression of CD8 T cell progenies generated via asymmetric cell division

Project description:Asymmetric partitioning of fate-determinants is a mechanism that contributes to T cell differentiation. However, it remained unclear whether the ability of T cells to divide asymmetrically is influenced by their differentiation state, as well as if enforcing asymmetric cell division rates would have an impact on T cell differentiation and memory formation. Using the murine LCMV infection model, we established a correlation between cell stemness and the ability of CD8+ T cells to undergo asymmetric cell division (ACD). Transient mTOR inhibition proved to increase ACD rates in naïve and memory cells, and to install this ability in exhausted CD8+ T cells. Functionally, enforced ACD correlated with increased memory potential, leading to more efficient recall response and viral control upon acute or chronic LCMV infection. Moreover, transient mTOR inhibition also increased ACD rates in human CD8+ T cells. Transcriptional profiling of first daughter cells, obtained by sorting CD8lo and CD8hi cells after in vitro stimulation, revealed that progenies emerging from enforced ACD exhibited more pronounced early memory signatures, which functionally endowed these cells with strengthened memory features.

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