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Changing the Waddington landscape to control mesendoderm competence -- ATAC-seq

ABSTRACT: Changing the Waddington landscape to control mesendoderm competence -- ATAC-seq

PROVIDER: PRJNA627245 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11584837_1.fastq.gz	Fastqsanger.gz
	SRR11584837_2.fastq.gz	Fastqsanger.gz
	SRR11584838_1.fastq.gz	Fastqsanger.gz
	SRR11584838_2.fastq.gz	Fastqsanger.gz
	SRR11584839_1.fastq.gz	Fastqsanger.gz

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Changing the Waddington landscape to control mesendoderm competence

Project description:Changing the Waddington landscape to control mesendoderm competence

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Changing the Waddington landscape to control mesendoderm competence -- ATAC-seq

Project description:As pluripotent human embryonic stem cells progress towards one germ layer fate, they lose the ability to adopt alternative fates. It is unknown how the cells’ competence for these alternative fates changes along their developmental trajectory or if this competence can be modulated. Here, we show that a differentiating stem cell’s probability of adopting a mesendodermal fate when given the appropriate signal falls sharply at a specific point along the ectodermal trajectory, and we further demonstrate that this point can be moved using genetic perturbations. Using a low-dimensional reaction coordinate to monitor progression towards ectoderm, we can determine the probability that individual cells at different points along this path can transition to the mesendodermal fate upon BMP4 and Activin A signal exposure. Knowing this probability allows us to prospectively isolate and profile differentiating cells based on their mesendoderm competence. Analysis and validation of these RNA-seq and ATAC-seq profiles identified transcription factors that can independently control the cell’s mesendoderm competence and its progression along the ectodermal developmental trajectory. In the classical picture of a Waddington landscape, these effects correspond to altering the barrier between fates and changing the cell’s location on the landscape, respectively. The ability of the underlying gene regulatory network to modulate these two aspects of the developmental landscape could allow separate control of the dynamics of differentiation and tissue size proportions.

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Changing the Waddington landscape to control mesendoderm competence -- RNA-seq

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Changing the Waddington landscape to control mesendoderm competence -- RNA-seq

Project description:Changing the Waddington landscape to control mesendoderm competence -- RNA-seq

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Project description:Changing the Waddington landscape to control mesendoderm competence

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Changing the Waddington landscape to control mesendoderm competence

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

2021-11-08 | GSE149078 | GEO

Mesendoderm induction

Project description:ES cells are differentiated into mesenderm cell linage by Activin A treatment. During this differentaition, gene expression profile of ES cells, day 4 mesendoderm cell, day 5 mesendoderm cells and mesoderm cells are examined.

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Sequential enhancer state remodelling defines human germline competence and specification [ATAC-seq]

Project description:Germline-soma segregation is a fundamental event during mammalian embryonic development. Here we establish the epigenetic principles of human primordial germ cell (hPGC) development using in vivo hPGCs and stem cell models recapitulating gastrulation. We show that morphogen-induced remodelling of mesendoderm enhancers transiently confers the competence for hPGC fate, but further activation favours mesoderm and endoderm fates. Consistently, reducing the expression of the mesendodermal transcription factor OTX2 promotes the PGC fate. In hPGCs, SOX17 and TFAP2C initiate activation of enhancers to establish a core germline programme, including the transcriptional repressor PRDM1 and pluripotency factors POU5F1 and NANOG. We demonstrate that SOX17 enhancers are the critical components in the regulatory circuitry of germline competence. Furthermore, activation of upstream cis-regulatory elements by an optimized CRISPR activation system is sufficient for hPGC specification. We reveal an enhancer-linked germline transcription factor network that provides the basis for the evolutionary divergence of mammalian germlines.

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