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ATAC-Seq of chicken embryonic metatarsal skin treated with RCAS-CTNNB1, RCAS-GFP, and retinoic acid

ABSTRACT: The molecular mechanism controlling regional specific skin appendage phenotypes is a fundamental question that remains unresolved. We recently identified feather and scale primordium associated genes and with functional studies, proposed five major more modules are involved in scale-to-feather conversion and their integration is essential to form today’s feathers. Yet, how the molecular networks are wired and integrated at the genomic level is still unknown. Here, we combine classical recombination experiments and systems biology technology to explore the molecular mechanism controlling cell fate specification. In the chimeric explant, dermal fate is more stable, while epidermal fate is reprogrammed to be similar to the original appendage type of the mesenchyme. We analyze the transcriptome changes in both scale-to-feather and feather-to-scale transition in the epidermis. We found a highly interconnected regulatory gene network controlling skin appendage types. These gene networks are organized around two molecular hubs, β-catenin and retinoic acid (RA), which can bind to regulatory elements controlling downstream gene expression, leading to scale or feather fates. ATAC sequencing analyses revealed about 1000 altered chromatin opening sites, and they are distributed around. When a key gene is perturbed, many other co-expressed genes in the same module also will be influenced. These findings suggest that these feather / scale fate specification genes form an interconnected network, and rewiring of the gene network can lead to changes of appendage phenotypes. This work shows the key hub positions of Beta catenin and retinoic acid signaling in the hierarchy of the scale / feather fate specification gene networks, opening up new possibilities to understand the control switches of multi-component organ phenotypes.

ORGANISM(S): Gallus gallus

PROVIDER: GSE111098 | GEO | 2018/10/15

REPOSITORIES: GEO

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Project description:Mbodj2016 - Mesoderm specification during Drosophila development This model is described in the article: Qualitative Dynamical Modelling Can Formally Explain Mesoderm Specification and Predict Novel Developmental Phenotypes. Mbodj A, Gustafson EH, Ciglar L, Junion G, Gonzalez A, Girardot C, Perrin L, Furlong EE, Thieffry D. PLoS Comput. Biol. 2016 Sep; 12(9): e1005073 Abstract: Given the complexity of developmental networks, it is often difficult to predict the effect of genetic perturbations, even within coding genes. Regulatory factors generally have pleiotropic effects, exhibit partially redundant roles, and regulate highly interconnected pathways with ample cross-talk. Here, we delineate a logical model encompassing 48 components and 82 regulatory interactions involved in mesoderm specification during Drosophila development, thereby providing a formal integration of all available genetic information from the literature. The four main tissues derived from mesoderm correspond to alternative stable states. We demonstrate that the model can predict known mutant phenotypes and use it to systematically predict the effects of over 300 new, often non-intuitive, loss- and gain-of-function mutations, and combinations thereof. We further validated several novel predictions experimentally, thereby demonstrating the robustness of model. Logical modelling can thus contribute to formally explain and predict regulatory outcomes underlying cell fate decisions. This model is hosted on BioModels Database and identified by: MODEL1607310000. To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

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ATAC-Seq of chicken embryonic metatarsal skin treated with RCAS-CTNNB1, RCAS-GFP, and retinoic acid

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