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Suppression of ERK signalling promotes pluripotent epiblast in the human blastocyst

ABSTRACT: Suppression of ERK signalling promotes pluripotent epiblast in the human blastocyst

PROVIDER: PRJNA1054619 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR25486800_1.fastq.gz	Fastqsanger.gz
	SRR25486800_2.fastq.gz	Fastqsanger.gz
	SRR25486803_1.fastq.gz	Fastqsanger.gz
	SRR25486803_2.fastq.gz	Fastqsanger.gz

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Suppression of ERK signalling promotes pluripotent epiblast in the human blastocyst

Project description:Suppression of ERK signalling promotes pluripotent epiblast in the human blastocyst

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Suppression of ERK signalling promotes pluripotent epiblast in the human blastocyst [mouse_ERKi_scRNAseq]

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Suppression of ERK signalling promotes pluripotent epiblast in the human blastocyst [RNA-seq I]

Project description:Studies in the mouse demonstrate the importance of fibroblast growth factor (FGF) and extra-cellular receptor tyrosine kinase (ERK) in specification of the epiblast and hypoblast in the inner cell mass (ICM). We recently demonstrated cross-talk of ERK and PI3K activity downstream of FGF and insulin growth factor signaling. We therefore hypothesized that ERK may have a conserved role in human hypoblast versus epiblast specification. Here we determined that FGF signaling is sufficient to specify hypoblast in human blastocysts. We describe ERK signaling during the blastocyst stage and demonstrate that blocking ERK activity, by small-molecule inhibition, is necessary for hypoblast specification in human blastocysts, and leads to expansion of the epiblast cells functionally capable of giving rise to naïve pluripotent embryonic stem cells. Transcriptomic analysis further reveals that these epiblast cells downregulate insulin growth factor and FGF signaling, while maintaining molecular markers of the epiblast. Moreover, we generate human naïve pluripotent stem cells following ERK inhibition. Our functional studies provide mechanistic insight into human blastocyst formation. We propose a unified model in which segregation of the epiblast and hypoblast lineages occurs during maturation of the mammalian blastocyst in an FGF/ERK signal-dependent manner.

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Suppression of ERK signalling promotes pluripotent epiblast in the human blastocyst [RNA-seq II]

Project description:Suppression of ERK signalling promotes pluripotent epiblast in the human blastocyst [RNA-seq II]

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Suppression of ERK signalling promotes pluripotent epiblast in the human blastocyst [RNA-seq I]

Project description:Suppression of ERK signalling promotes pluripotent epiblast in the human blastocyst [RNA-seq I]

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Suppression of ERK signalling promotes pluripotent epiblast in the human blastocyst

Project description:Studies in the mouse demonstrate the importance of fibroblast growth factor (FGF) and extra-cellular receptor tyrosine kinase (ERK) in specification of embryo-fated epiblast and yolk-sac-fated hypoblast cells from uncommitted inner cell mass (ICM) cells prior to implantation. Molecular mechanisms regulating specification of early lineages in human development are comparatively unclear. Here we show that exogenous FGF stimulation leads to expanded hypoblast molecular marker expression, at the expense of the epiblast. Conversely, we show that specifically inhibiting ERK activity leads to expansion of epiblast cells functionally capable of giving rise to naïve human pluripotent stem cells. Single-cell transcriptomic analysis indicates that these epiblast cells downregulate FGF signalling and maintain molecular markers of the epiblast. Our functional study demonstrates the molecular mechanisms governing ICM specification in human development, whereby segregation of the epiblast and hypoblast lineages occurs during maturation of the mammalian embryo in an ERK signal-dependent manner.

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Suppression of ERK signalling promotes pluripotent epiblast in the human blastocyst [mouse_ERKi_scRNAseq]

Project description:Studies in the mouse demonstrate the importance of fibroblast growth factor (FGF) and extra-cellular receptor tyrosine kinase (ERK) in specification of embryo-fated epiblast and yolk-sac-fated hypoblast cells from uncommitted inner cell mass (ICM) cells prior to implantation. Molecular mechanisms regulating specification of early lineages in human development are comparatively unclear. Here we show that exogenous FGF stimulation leads to expanded hypoblast molecular marker expression, at the expense of the epiblast. Conversely, we show that specifically inhibiting ERK activity leads to expansion of epiblast cells functionally capable of giving rise to naïve human pluripotent stem cells. Single-cell transcriptomic analysis indicates that these epiblast cells downregulate FGF signalling and maintain molecular markers of the epiblast. Our functional study demonstrates the molecular mechanisms governing ICM specification in human development, whereby segregation of the epiblast and hypoblast lineages occurs during maturation of the mammalian embryo in an ERK signal-dependent manner.

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Project description:Studies in the mouse demonstrate the importance of fibroblast growth factor (FGF) and extra-cellular receptor tyrosine kinase (ERK) in specification of embryo-fated epiblast and yolk-sac-fated hypoblast cells from uncommitted inner cell mass (ICM) cells prior to implantation. Molecular mechanisms regulating specification of early lineages in human development are comparatively unclear. Here we show that exogenous FGF stimulation leads to expanded hypoblast molecular marker expression, at the expense of the epiblast. Conversely, we show that specifically inhibiting ERK activity leads to expansion of epiblast cells functionally capable of giving rise to naive human pluripotent stem cells. Single-cell transcriptomic analysis indicates that these epiblast cells downregulate FGF signalling and maintain molecular markers of the epiblast. Our functional study demonstrates the molecular mechanisms governing ICM specification in human development, whereby segregation of the epiblast and hypoblast lineages occurs during maturation of the mammalian embryo in an ERK signal-dependent manner.

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