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WNT signaling memory is required for ACTIVIN to function as a morphogen

ABSTRACT: WNT signaling memory is required for ACTIVIN to function as a morphogen

PROVIDER: PRJNA437954 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6826330_1.fastq.gz	Fastqsanger.gz
	SRR6826330_2.fastq.gz	Fastqsanger.gz
	SRR6826331_1.fastq.gz	Fastqsanger.gz
	SRR6826331_2.fastq.gz	Fastqsanger.gz
	SRR6826332_1.fastq.gz	Fastqsanger.gz

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WNT signaling memory is required for ACTIVIN to function as a morphogen

Project description:It has now become clear that the process of fate specification during early embryogenesis is mediated by a handful of key signaling pathways. However, how the temporal and spatial integration of these signals plays out to give rise to self-organization of tissues remains obscure. Here we use artificial human gastruloids and quantitative single-cell analysis to dissect the temporal integration of two key pathways WNT and ACTIVIN that along with BMP control gastrulation and primitive streak patterning in model systems. We showed that ACTIVIN elicits a transient signaling response, as well as a transient induction of differentiation. However, unlike BMP and WNT, ACTIVIN cannot induce stable primitive streak formation and mesodermal patterning. Pre-exposure to WNT switches the response of cells to ACTIVIN whereby it becomes a concentration dependent morphogen. This provides evidence for WNT signaling memory that occurs at the transcriptional level and not as a modifier of ACTIVIN signaling dynamics.

2018-10-22 | GSE111717 | GEO

Gene expression profile of cells with unfit Wnt morphogen gradient during cell competition

Project description:Morphogen signalling forms an activity gradient and instructs cell identities in a signalling strength-dependent manner to pattern developing tissues. However, developing tissues also undergo dynamic morphogenesis, which may produce cells with unfit morphogen signalling and consequent noisy morphogen gradient. Here we show that a cell competition-related system corrects such noisy morphogen gradients. Zebrafish imaging analyses of the Wnt/β-catenin signalling gradient, which acts as a morphogen to establish embryonic anterior-posterior patterning, revealed that unfit cells with abnormal Wnt/β-catenin activity spontaneously appear and produce noise in the gradient. Communication between unfit and neighbouring fit cells via cadherin proteins stimulates apoptosis of the unfit cells by activating Smad signalling and reactive oxygen species production. This unfit cell elimination is required for proper Wnt/β-catenin gradient formation and consequent anterior-posterior patterning. Because this gradient controls patterning not only in the embryo but also in adult tissues, this system may support tissue robustness and disease prevention.

2019-09-15 | GSE133526 | GEO

Gene expression profile of neighboring cells of cells with unfit Wnt morphogen gradient during cell competition

2024-11-15 | GSE254439 | GEO

WNT signaling memory is required for ACTIVIN to function as a morphogen in human gastruloids.

Project description:Self-organization of discrete fates in human gastruloids is mediated by a hierarchy of signaling pathways. How these pathways are integrated in time, and whether cells maintain a memory of their signaling history remains obscure. Here, we dissect the temporal integration of two key pathways, WNT and ACTIVIN, which along with BMP control gastrulation. CRISPR/Cas9-engineered live reporters of SMAD1, 2 and 4 demonstrate that in contrast to the stable signaling by SMAD1, signaling and transcriptional response by SMAD2 is transient, and while necessary for pluripotency, it is insufficient for differentiation. Pre-exposure to WNT, however, endows cells with the competence to respond to graded levels of ACTIVIN, which induces differentiation without changing SMAD2 dynamics. This cellular memory of WNT signaling is necessary for ACTIVIN morphogen activity. A re-evaluation of the evidence gathered over decades in model systems, re-enforces our conclusions and points to an evolutionarily conserved mechanism.

| S-EPMC6234031 | biostudies-literature

RNA- and ATAC-seq data from hESCs differentiated with Wnt and Activin with or without CPI-203

Project description:We report genome-wide changes in chromatin state and transcriptional output following Wnt-priming and subsequent Activin induced differentiation of human embryonic stem cell and the effects of BET bromodomain inhibition during Wnt-priming. The two signals, Wnt and Activin, although provided sequentially, result in stable mesendoderm differentiation (Yoney et al., 2018).

2021-06-06 | GSE176222 | GEO

Activin/Smad2 and Wnt/β-catenin upregulate HAS2 and ALDH3A2 to facilitate mesendoderm differentiation of human ESCs

Project description:Activin and Wnt signaling are necessary and sufficient for mesendoderm (ME) differentiation of human embryonic stem cells (hESCs). In this study, we report that during the Activin and Wnt induced ME differentiation, Activin/Smad2 induces decrease of the repressive histone modification H3K27me3 by promoting proteasome-dependent degradation of EZH2. As a result, recruitment of the forkhead protein FOXH1 on open chromatin regions integrates the signals of Activin/Smad2 and Wnt/β-catenin to activate the expression of the ME genes including HAS2 and ALDH3A2. Knockdown of HAS2 and ALDH3A2 greatly attenuates ME differentiation. These findings unveil a pathway from extracellular signals to epigenetic modification-mediated gene activation during ME commitment.

2018-09-29 | GSE113047 | GEO

Gene expression profile of cells with unfit Wnt morphogen gradient during cell competition

Project description:Gene expression profile of cells with unfit Wnt morphogen gradient during cell competition

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Morphogen Stimulated Endocytic Recycling Drives Cytoneme Loading for Mammalian Tissue Patterning

Project description:During development, morphogens build tissues by instructing cell fate across long distances. Directly visualizing morphogen transport in situ has been unfeasible, so the molecular mechanisms ensuring successful morphogen delivery remain unclear. To tackle this longstanding problem, we developed a mouse model for compromised Sonic Hedgehog (SHH) morphogen delivery and discovered that endocytic recycling promotes SHH loading into signaling filopodia called cytonemes. We optimized methods to preserve in vivo cytonemes for advanced microscopy and show endogenously-expressed SHH localized to cytonemes in developing mouse neural tubes. Depletion of SHH from neural tube cytonemes alters neuronal cell fates and compromises neurodevelopment. Mutation of the filopodial motor Myosin 10 (MYO10) reduces cytoneme length and density, which corrupts neuronal signaling activity of both SHH and WNT. Combined, these results demonstrate that cytoneme-based signal transport provides essential contributions to morphogen dispersion during mammalian tissue development and suggest MYO10 is a key regulator of cytoneme function.

2024-01-02 | GSE242161 | GEO

Activin A is Required for the Self-Renewal of Aortic Sox2+ Neurospheres

Project description:Activin A is Required for the Self-Renewal of Aortic Sox2+ Neurospheres

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Gene expression profile of neighboring cells of cells with unfit Wnt morphogen gradient during cell competition

Project description:Gene expression profile of neighboring cells of cells with unfit Wnt morphogen gradient during cell competition

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