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Spatial transcriptome profiling by MERFISH reveals fetal liver hematopoietic stem cell niche architecture.

ABSTRACT: Spatial transcriptome profiling by MERFISH reveals fetal liver hematopoietic stem cell niche architecture.

PROVIDER: PRJNA722179 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14243162_1.fastq.gz	Fastqsanger.gz
	SRR14243162_2.fastq.gz	Fastqsanger.gz
	SRR14243171_1.fastq.gz	Fastqsanger.gz
	SRR14243171_2.fastq.gz	Fastqsanger.gz
	SRR14243172_1.fastq.gz	Fastqsanger.gz

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Spatial transcriptome profiling by MERFISH reveals fetal liver hematopoietic stem cell niche architecture [scRNA-seq]

Project description:The hematopoietic stem cell (HSC) niche has been extensively studied in bone marrow, yet a more systematic investigation into the microenvironment regulation of hematopoiesis in fetal liver is necessary. Here we investigate the spatial organization and transcriptional profile of individual cells in both wild type and Tet2-/- fetal livers, by multiplexed error robust fluorescence in situ hybridization (MERFISH). We find that specific pairs of fetal liver cell types are preferentially positioned next to each other. Ligand-receptor singling molecule pairs such as Kitl and Kit are enriched in neighboring cell types. The majority of HSCs are directly in contact with endothelial cells (ECs) in both wild type and Tet2-/- fetal livers. Loss of Tet2 increases the number of HSCs, and upregulates Wnt and Notch signaling genes in the HSC niche. Two subtypes of ECs – arterial ECs and sinusoidal ECs – and other cell types contribute distinct signaling molecules to the HSC niche. Collectively, this study provides a comprehensive picture and bioinformatic foundation for HSC spatial regulation in fetal liver.

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Project description:Preterm infants are at risk for brain injury and long term neurodevelopmental impairment due, in part, to white matter injury following chronic hypoxia exposure. However, the precise molecular mechanisms by which perinatal hypoxia disrupts early neurodevelopment are poorly understood. Here, we constructed a brain-wide map of the regenerative response to newborn brain injury using high resolution imaging-based spatial transcriptomics (MERFISH) to analyze over 1.3 million cells in a mouse model of chronic neonatal hypoxia. We also developed a new method for inferring condition-associated differences in cell type spatial proximity, enabling the identification of niche-specific changes in cellular architecture. We observed significant hypoxia-associated changes in region-specific cell states, cell type composition, and spatial organization. Our findings suggest that perinatal hypoxia disrupts oligodendrocyte formation and crosstalk signaling with other cell types in their niche. Importantly, our analysis of spatially-informed gene expression patterns revealed specific mechanisms of reparative neurogenesis and gliogenesis, and nominated pathways that may impede circuit rewiring following perinatal hypoxia. Altogether, our work provides a comprehensive description of the brain-wide response to newborn brain injury and identifies candidate signaling pathways for functional interrogation.

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Spatial transcriptome profiling by MERFISH reveals fetal liver hematopoietic stem cell niche architecture.

Project description:The hematopoietic stem cell (HSC) niche has been extensively studied in bone marrow, yet a more systematic investigation into the microenvironment regulation of hematopoiesis in fetal liver is necessary. Here we investigate the spatial organization and transcriptional profile of individual cells in both wild type (WT) and Tet2-/- fetal livers, by multiplexed error robust fluorescence in situ hybridization. We find that specific pairs of fetal liver cell types are preferentially positioned next to each other. Ligand-receptor signaling molecule pairs such as Kitl and Kit are enriched in neighboring cell types. The majority of HSCs are in direct contact with endothelial cells (ECs) in both WT and Tet2-/- fetal livers. Loss of Tet2 increases the number of HSCs, and upregulates Wnt and Notch signaling genes in the HSC niche. Two subtypes of ECs, arterial ECs and sinusoidal ECs, and other cell types contribute distinct signaling molecules to the HSC niche. Collectively, this study provides a comprehensive picture and bioinformatic foundation for HSC spatial regulation in fetal liver.

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Spatial transcriptome profiling by MERFISH reveals fetal liver hematopoietic stem cell niche architecture.

Project description:This SuperSeries is composed of the SubSeries listed below.

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