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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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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.

2009-06-12 | E-MEXP-1672 | biostudies-arrayexpress

RNAseq and ChIPseq on Mouse Embryonic Stem Cells and Sorted Mesendoderm Progenitor Cells [RNA-seq]

Project description:We mapped the enhancer and long non-coding transcriptional landscape during mesendoderm specification. Mesendodermal progenitors were sorted from differentiating ESCs according to Eomes expression. Enhancer usage was coordinated with mesendoderm-specific expression of key lineage-determining transcription factors. We demonstrated that many of these enhancers are associated with the expression of lncRNAs.

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A novel role for ASCL1 in the regulation of mesendoderm formation via HDAC-dependent antagonism of VegT function

Project description:Maternally expressed proteins function in vertebrates to establish the major body axes of the embryo, and to establish a pre-pattern that sets the stage for later acting zygotic signals. This pre-pattern drives the propensity of Xenopus animal cap cells to adopt neural fates under various experimental conditions. Previous studies found that the maternally expressed transcription factor, encoded by the Xenopus achaete-scute like gene ascl1, is enriched at the animal pole. Asc1l is a bHLH protein involved in neural development, but its maternal function has not been studied. In this study, we have performed a series of gain and loss of function experiments on maternal ascl1, and present three novel findings. First, Ascl1 is a repressor of mesendoderm induced by VegT, but not of Nodal induced mesendoderm. Secondly, a previously uncharacterized N-terminal domain of Ascl1 interacts with HDAC1 to inhibit mesendoderm gene expression. This N-terminal domain is dispensable for its neurogenic function, indicating that Ascl1 has acts by different mechanisms at different times. Ascl1-mediated repression of mesendoderm genes was dependent on HDAC activity and accompanied by histone deacetylation in the promoter regions of VegT targets. Finally, maternal Ascl1 is required for animal cap cells to retain their competence to adopt neural fates. These results establish maternal Asc1l as a key factor in establishing the pre-pattern of the early embryo, acting in opposition to VegT and biasing the animal pole to adopt neural fates. The data presented here significantly extend our understanding of early embryonic pattern formation. Examination of genes expression in control (cMO) and Ascl1 MO knockdown (AMOs) embryos by deep sequencing.

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