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Principles of Signalling Pathway Modulation for Enhancing Human Naïve Pluripotency Induction [ChIP-seq]

ABSTRACT: Principles of Signalling Pathway Modulation for Enhancing Human Naïve Pluripotency Induction [ChIP-seq]

PROVIDER: PRJNA516809 | ENA |

REPOSITORIES: ENA

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Principles of Signalling Pathway Modulation for Enhancing Human Naïve Pluripotency Induction

Project description:Principles of Signalling Pathway Modulation for Enhancing Human Naïve Pluripotency Induction

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Principles of Signalling Pathway Modulation for Enhancing Human Naïve Pluripotency Induction [WGBS]

Project description:Principles of Signalling Pathway Modulation for Enhancing Human Naïve Pluripotency Induction [WGBS]

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Principles of Signalling Pathway Modulation for Enhancing Human Naïve Pluripotency Induction [ATAC-Seq]

Project description:Principles of Signalling Pathway Modulation for Enhancing Human Naïve Pluripotency Induction [ATAC-Seq]

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Principles of Signalling Pathway Modulation for Enhancing Human Naïve Pluripotency Induction [RNA-seq]

Project description:Principles of Signalling Pathway Modulation for Enhancing Human Naïve Pluripotency Induction [RNA-seq]

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Principles of Signalling Pathway Modulation for Enhancing Human Naïve Pluripotency Induction [WGBS]

Project description:Isolating human MEK/ERK signalling independent pluripotent stem cells (PSCs) with characteristics of naive pluripotency while maintaining differentiation competence and genetic integrity, remains challenging. Here we engineer reporter systems that allow screening for conditions that induce molecular and functional features of human naive pluripotency. Synergistic inhibition of WNT-ßCATENIN, PKC and SRC signalling enables induction of teratoma competent naïve human PSCs, with capacity to differentiate into trophoblast stem cells (TSC) and extraembryonic endodermal (XEN) cells in vitro. Divergent signalling and transcriptional requirements for boosting naïve pluripotency were found between mouse and human. P53 depletion in human naïve PSCs endows them with competitiveness to better contribute to mouse-human cross-species chimeric embryos upon priming. Finally, MEK/ERK inhibition can be substituted with inhibition for NOTCH/RBPj, which allows inducing alternative human naïve-like PSCs with diminished risk for deleterious global DNA hypomethylation. Our findings set a framework for defining the signalling foundations of human naïve pluripotency.

2021-03-25 | GSE142812 | GEO

Principles of Signalling Pathway Modulation for Enhancing Human Naïve Pluripotency Induction [ChIP-seq]

2021-03-25 | GSE125553 | GEO

Principles of Signalling Pathway Modulation for Enhancing Human Naïve Pluripotency Induction [ATAC-Seq]

2021-03-25 | GSE124614 | GEO

Principles of Signalling Pathway Modulation for Enhancing Human Naïve Pluripotency Induction [RNA-seq]

2021-03-25 | GSE150772 | GEO

Principles of Signalling Pathway Modulation for Enhancing Human Naïve Pluripotency Induction

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

2021-03-25 | GSE125555 | GEO

Naïve human pluripotency stem cells respond to Wnt, Nodal and LIF signalling to produce expandable naïve extra-embryonic endoderm

Project description:Embryonic stem cells (ESCs) can exist in at least two states that transcriptionally resemble different stages of embryonic development. Naïve ESCs resemble peri-implantation stages and primed ESCs the pre-gastrulation epiblast. In mouse, primed ESCs give rise to definitive endoderm in response to pathways downstream of Nodal and Wnt signalling. However, when these cytokines are applied to naïve ESCs, they differentiate to a cell type that approximates early primitive endoderm (PrE), the blastocyst stage progenitor layer that gives rise to the extra-embryonic endoderm. Here, we apply this context dependency to human ESCs, showing that these cytokines drive the differentiation of naïve pluripotent cells to generate extra-embryonic PrE, or hypoblast, and, as in mouse, expanded as an in vitro model for naïve extra-embryonic endoderm (nEnd) in defined conditions. Consistent with observations made in mouse, human PrE differentiation is dependent on FGF signalling in vitro, and we show, that by inhibiting FGF receptor signalling, we could simplify naïve pluripotent culture such that inhibitor requirements closer resembled those used in mouse. These nEnd cultures represent stable extra-embryonic endoderm, or human hypoblast, cell lines.

2019-11-30 | GSE138012 | GEO

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