Abstract
The epidermal differentiation complex (EDC) encodes a group of unique proteins expressed in late epidermal differentiation. The EDC gave integuments new physicochemical properties and is critical in evolution. Recently, we showed β-keratins, members of the EDC, undergo gene cluster switching with overexpression of SATB2 (Special AT-rich binding protein-2), considered a chromatin regulator. We wondered whether this unique regulatory mechanism is specific to β-keratins or may be derived from and common to EDC members. Here we explore (1) the systematic expression patterns of non-β-keratin EDC genes and their preferential expression in different skin appendages during development, (2) whether the expression of non-β-keratin EDC sub-clusters are also regulated in clusters by SATB2. We analyzed bulk RNA-seq and ChIP-seq data and also evaluated the disrupted expression patterns caused by overexpressing SATB2. The results show that the expression of whole EDDA and EDQM sub-clusters are possibly mediated by enhancers in E14-feathers. Overexpressing SATB2 down-regulates the enriched EDCRP sub-cluster in feathers and the EDCH sub-cluster in beaks. These results reveal the potential of complex epigenetic regulation activities within the avian EDC, implying transcriptional regulation of EDC members acting at the gene and/or gene cluster level in a temporal and skin regional-specific fashion, which may contribute to the evolution of diverse avian integuments.
Highlights
Skin, composed of several region-specific differentiated epidermis forms, acts as a barrier protecting the body from external environmental assaults including biological, physical, and chemical attacks
A gene cluster located within the gene locus known as the epidermal differentiation complex (EDC) encodes many proteins involved in late embryonic epidermal differentiation [2]
In the UCSC chicken galGal6 (GRC6a) chicken genome, the EDC gene organization on Chromosome 25 (Chr25) is separated into two parts within 1300 kb (Figure 1a)
Summary
Skin, composed of several region-specific differentiated epidermis forms, acts as a barrier protecting the body from external environmental assaults including biological, physical, and chemical attacks. The cornified outer layer of the skin in the stratum corneum is composed of dead keratinocytes. This epithelial layer develops at the end of epidermal differentiation due to keratinocyte keratinization and cell death [1]. FLG mutations lead to ichthyosis vulgaris, in which the granular layer is reduced, and hyperkeratosis is prevalent. Both characteristics are strongly associated with atopic dermatitis (AD) and AD-associated asthma [4,5,6,7,8]
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