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Selective activation of FZD7 in human pluripotent stem cells

ABSTRACT: Selective activation of FZD7 in human pluripotent stem cells

PROVIDER: PRJNA664040 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12659730_1.fastq.gz	Fastqsanger.gz
	SRR12659730_2.fastq.gz	Fastqsanger.gz
	SRR12659731_1.fastq.gz	Fastqsanger.gz
	SRR12659731_2.fastq.gz	Fastqsanger.gz
	SRR12659732_1.fastq.gz	Fastqsanger.gz

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Selective activation of FZD7 in human pluripotent stem cells

Project description:Human pluripotent stem cells ( (H1/WA01/NIH stem cell registry number 0043) were treated with WNT3a protein, a FZD7-specific WNT mimetic, and a GSK3 inihibitor in time series to determine genes differentially upregulated and downregulated across all conditions or within one condition only.

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Selective activation of FZD2 and FZD7 reveals non-redundant function during mesoderm differentiation

Project description:Wnt-ßcatenin signalling controls stem cell self-renewal and cell fate decisions and therefore its precise control could influence differentiation protocols efficiency and cell therapy efforts. During gastrulation, Wnt-ßcatenin signalling dictates lineage bifurcation choices leading from pluripotency to distinct primitive streak patterning, ultimately resulting in various mesendoderm cell types. However, the nature of the Wnt receptors involved in this process and how their signaling dynamics impact mesoderm specification remain elusive. Here, we used selective Frizzled and LRP5/6 antibody-based agonists (FLAgs) to investigate the function and activation kinetics of Frizzled receptor complexes during directed mesoderm differentiation of hPSCs. We found that FZD2 and FZD7 are expressed at the surface of hPSCs and that their activation triggers ßcatenin signaling with different kinetics thereby influencing mesoderm patterning choices. Using bulk and single-cell RNA sequencing, we showed that FZD7 activation promotes lineage commitment towards both paraxial and lateral mesoderm whereas FZD2 engagement preferentially induces paraxial mesoderm. Mechanistically, our results demonstrate that although the short-term response following FZD2 and FZD7 activation is similar, ßcatenin signaling kinetics differs. FZD2 activation results in a sustained Wnt activation profile that drives hPSCs differentiation to paraxial mesoderm while blocking lateral mesoderm. In contrast, FZD7 activation kinetics consists of a similar initial activation followed by dampening of the response to a low level of ßcatenin signaling that is permissive for lateral mesoderm induction in addition to paraxial mesoderm specification. Our results suggest that the function of FZD2 and FZD7 during mesoderm specification is non-redundant and that their selective activation to temporally modulate Wnt-ßcatenin signaling can be leveraged for precise directed differentiation outcomes.

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Selective activation of FZD2 and FZD7 reveals non-redundant function during mesoderm differentiation

Project description:Selective activation of FZD2 and FZD7 reveals non-redundant function during mesoderm differentiation

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Project description:mouse embryonic fibroblasts, embryonic stem cells, and induced pluripotent stem cells were compared via metabolomic analysis

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Expression data from human pluripotent stem cells and differentiated cells treated with pluripotent-specific inhibitors

Project description:The use of human pluripotent stem cells (hPSCs) in cell therapy is hindered by the tumorigenic risk from residual undifferentiated cells. Here we performed a high-throughput screen of over 52,000 small molecules, and identified 15 highly selective cytotoxic inhibitors of hPSCs (PluriSIns). Cellular and molecular analyses revealed that the most selective compound, PluriSIn #1, is a pluripotent-specific inhibitor of stearoyl-coA desaturase (SCD1), the key enzyme in the biosynthesis of monounsaturated fatty acids (MUFA). SCD1 inhibition in hPSCs induced ER stress, protein synthesis attenuation, and apoptosis of these cells, revealing that MUFA biosynthesis is crucial for their survival. PluriSIn #1 was also cytotoxic toward the ICM cells of mouse embryos, indicating that the dependence on SCD1 is inherent to the pluripotent state. Finally, application of PluriSIn #1 prevented teratoma formation from tumorigenic undifferentiated cells. Our novel method to eliminate undifferentiated cells from culture should thus increase the safety of hPSC-based treatments. Expression data from undifferentiated and differentiated human embryonic stem cells. Total RNA was isolated from undifferentiated human pluripotent stem cells grown on matrigel with mTeSR1 medium, or from early endodermal progenitor cells differentiated from human embryonic stem cells.

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Project description:CRISPR activation enables high fidelity reprogramming into human pluripotent stem cells (single cells)

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Project description:Pluripotent stem cells are defined by their self-renewal capacity, which is the ability of the stem cells to proliferate indefinitely while maintaining the pluripotent identity essential for their ability to differentiate into any somatic cell lineage. However, understanding the mechanisms that control stem cell fitness versus the pluripotent cell identity is challenging. To investigate the interplay between these two aspects of pluripotency, we performed four parallel genome-scale CRISPR-Cas9 loss-of-function screens interrogating stem cell fitness in hPSC self-renewal conditions, and the dissolution of the primed pluripotency identity during early differentiation. Comparative analyses led to the discovery of genes with distinct roles in pluripotency regulation, including mitochondrial and metabolism regulators crucial for stem cell fitness, and chromatin regulators that control pluripotent identity during early differentiation. We further discovered a core set of factors that control both stem cell fitness and pluripotent identity, including a network of chromatin factors that safeguard pluripotency. Our unbiased and systematic screening and comparative analyses disentangle two interconnected aspects of pluripotency, provide rich datasets for exploring pluripotent cell identity versus cell fitness, and offer a valuable model for categorizing gene function in broad biological contexts.

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