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Expression data from embryonic chicken feather and scale skins

ABSTRACT: Epithelial appendages are the product of epithelial – mesenchymal interactions. Tissue recombination experiments showed that in general, the dermis determines the phenotype of the epithelial appendage. Chicken dorsal skin epithelium interacts with its underlying mesenchyme to form feathers beginning at E7 (H&H stage 31), while metatarsal scale epithelium interacts with its mesenchyme to form scales beginning at E9 (H&H stage 35) which stabilize around E12 (H&H stage 38). We sought to evaluate the molecular differences of tissues with different competence and inductive abilities to form feathers and scales. Chicken embryos were selected to obtain competent E7 and non-competent at E9 feather forming skin from dorsal. The competent E9 and non-competent E11 meta-tarsal scale forming skin from metatarsal were selected for examing the differences in regional specificity. Epithelium and mesenchyme from each skin were prepared separately. Samples were prepared for RNA extraction and hybridization on Affymetrix microarrays. We gathered 8 sets of samples for the analysis: undifferentiated E7 feather skin epithelium (E7fe) and mesenchyme (E7fm); differentiated E9 feather skin epithelium (E9fe) and mesenchyme (E9fm); undifferentiated E9 scale skin epithelium (E9se) and mesenchyme (E9sm); and differentiated E11 scale skin epithelium (E11se) and mesenchyme (E11sm)

ORGANISM(S): Gallus gallus

SUBMITTER: Michael Hughes

PROVIDER: E-GEOD-62882 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from embryonic chicken feather and scale skins

Project description:Epithelial appendages are the product of epithelial – mesenchymal interactions. Tissue recombination experiments showed that in general, the dermis determines the phenotype of the epithelial appendage. Chicken dorsal skin epithelium interacts with its underlying mesenchyme to form feathers beginning at E7 (H&H stage 31), while metatarsal scale epithelium interacts with its mesenchyme to form scales beginning at E9 (H&H stage 35) which stabilize around E12 (H&H stage 38). We sought to evaluate the molecular differences of tissues with different competence and inductive abilities to form feathers and scales.

2015-07-01 | GSE62882 | GEO

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RNA-Seq of chicken embryonic feather/scale recombination skin explants

Project description: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.

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Chicken embryonic E16 scutate scale and feather samples

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Regional specific differentiation of integumentary organs: SATB2 is involved in α- and β-keratin gene cluster switching in the chicken

Project description:Animals develop skin regional specificities to best adapt to their environments. Birds are excellent models in which to study the epigenetic mechanisms that facilitate these adaptions. Patients suffering from SATB2 mutations exhibit multiple defects including ectodermal dysplasia-like changes. The preferential expression of SATB2, a chromatin regulator, in feather-forming compared to scale-forming regions, suggests it functions in regional specification of chicken skin appendages by acting on either differentiation or morphogenesis. Retrovirus mediated SATB2 misexpression in developing feathers, beaks, and claws causes epidermal differentiation abnormalities (e.g. knobs, plaques) with few organ morphology alterations. Chicken β-keratins are encoded in 5 sub-clusters (Claw, Feather, Feather-like, Scale, and Keratinocyte) on Chromosome 25 and a large Feather keratin cluster on Chromosome 27. Type I and II α-keratin clusters are located on Chromosomes 27 and 33, respectively. Transcriptome analyses showed these keratins 1) are often tuned up or down collectively as a sub-cluster, and 2) these changes occur in a temporo-spatial specific manner. This cluster-level suppression is also seen in MMPs on Chromosome 1. SATB2 alters gene expression changes of most other transcripts without this cluster-level switching. These results suggest an organizing role of SATB2 in cluster-level gene co-regulation during skin regional specification.

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