Abortive placode formation in the feather tract of the scaleless chicken embryo

Abstract

The featherless phenotype of the scaleless mutant provides a model for delineating the process of feather follicle formation. Initial studies established that the mutation affects the epidermis and suggested that epidermis is unable to respond to signals from underlying dermis, or propagate a reciprocal signal. The work presented here demonstrates that scaleless epidermis does indeed respond to the initial inductive signals from dermis, as indicated by the localization of nuclear ␤-catenin and transient focal expression of genes expressed in the placode of wild-type feather rudiments. In the sporadic "escaper" feathers that form in scaleless, expression of many genes associated with the progression of feather development is comparable to that in wild-type embryos. An exception is the ectodysplasin receptor gene Edar, which is expressed at lower levels in mutant feather buds. These observations suggest that the scaleless mutation impairs the locally augmented expression of Edar required to stabilize the placodal fate and sustain feather development. Developmental Dynamics 236:3020 -3030, 2007.

Generation and Characterization of Function-blocking Anti-ectodysplasin A (EDA) Monoclonal Antibodies That Induce Ectodermal Dysplasia

“…These antibodies can thus probably be used to study EDA function in a wide range of species not necessarily easily amenable to genetic manipulations. Of particular relevance, chicken is used as a model for the study of feather development, and EDA is involved in this process (39,40). Based on the careful sequence analysis of EDA, EDAR, XEDAR, and TROY in various species, it has been hypothesized that TROY might be the receptor for EDA2 in vertebrates, with the exception of therians (i.e., marsupials and placental mammals) where the specificity of EDA2 would have shifted to XEDAR.…”

The Dermal Papilla: An Instructive Niche for Epithelial Stem and Progenitor Cells in Development and Regeneration of the Hair Follicle

“…FGFs expressed by the epidermal placode play a central role in recruiting dermal cells to condense beneath it (Song et al 1996(Song et al , 2004Wells et al 2012;Huh et al 2013). In mice or chickens harboring a mutation in FGF-20, the dermal condensate does not form, and although initial patterned expression of epidermal placode genes occurs, it does not fully resolve to a restricted pattern and subsequently fades as both epidermal and dermal cells adopt interfollicular fates (Houghton et al 2007;Huh et al 2013). These and other mutants that show transient epidermal patterning before a block of follicle maturation show that active communication between the epithelial and mesenchymal components of the nascent follicle are required to maintain initial fate decisions.…”

“…Multiple independent cells coalesce to form each DP (Collins et al 2012). The dermal condensate fate is plastic and can be reversed after initial specification, either in mutants in which developmental progression is blocked or in tissue reconstruction experiments with dissociated dermal cells (Jiang et al 1999;Houghton et al 2007). If there is subset of dermal cells specifically competent to become DP, it is larger than those that normally adopt this fate.…”

“…Global expression profiles reveal dynamic expression of secreted molecules in the DP during the hair cycle Rendl et al 2005;Driskell et al 2009;Greco et al 2009). Both interspecific tissue recombination experiments between epidermis and dermis and analysis of specific signaling pathways in different species have indicated that the mechanisms guiding early development of epidermal appendages are broadly conserved across taxonomic classes, including birds and mammals (Dhouailly 1973;Song et al 1996Song et al , 2004Jung et al 1998;Morgan et al 1998;Noramly and Morgan 1998;Jiang et al 1999;Noramly et al 1999;Laurikkala et al 2002;Houghton et al 2005Houghton et al , 2007Drew et al 2007;Wells et al 2012;Huh et al 2013). Thus, DP extirpation and reengraftment experiments that showed a requirement for the DP in the growth and regrowth of feathers implied a similar requirement for the DP in normal hair follicle growth and regeneration (Lillie and Wang 1941;Wang 1943).…”

Genomic determinants of epidermal appendage patterning and structure in domestic birds

“…Perhaps one of the most dramatic examples of variation in macropatterning is the scaleless ( sc locus) trait in chicken, a recessive mutation that causes a nearly complete lack of feathers and scales on the body due to a failure of placode formation during embryogenesis. For more than 50 years, researchers have utilized sc/sc mutant chickens as a model to study tissue interactions during skin development; dermal-epidermal recombination experiments using wild type and sc/sc tissue led to the discovery that the scaleless phenotype results from an inability of the epidermis to sustain a response to dermal patterning signals (Abbott and Asmundson, 1957; Brotman, 1977; Dhouailly and Sawyer, 1984; Houghton et al, 2007; Sengel and Abbott, 1963). Despite a strong mechanistic understanding of the developmental events that are altered during epidermal morphogenesis in sc/sc chickens, the molecular identity of sc was identified only recently.…”