The Edar subfamily in feather placode formation.
Open accessAbstract
A subgroup of the TNF receptor family, composed of Edar, Troy and Xedar, are implicated in the development of ectodermal appendages, such as hair follicles, teeth and sweat glands. We have isolated chicken orthologues of these three receptors and analysed their roles in early feather development. Conservation of protein sequences between mammalian and avian proteins is variable, with avian Edar showing the greatest degree of sequence identity. cXedar differs from its mammalian orthologue in that it contains an intracellular death domain. All three receptors are expressed during early feather morphogenesis and dominant negative forms of each receptor impair the epithelial contribution to feather bud morphogenesis, while the dermal contribution appears unaffected. Hyperactivation of each receptor leads to more widespread assumption of placode fate, though in different regions of the skin. Receptor signaling converges on NF-kappaB, and inhibiting this transcription factor alters feather bud number and size in a stage-specific manner. Our findings illustrate the roles of these three receptors during avian skin morphogenesis and also suggest that activators of feather placode fate undergo mutual regulation to reach a decision on skin appendage location and size.
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Eda signaling is necessary for the development and patterning of epithelial placodes of many integumentary organs in both mouse and chick.
“Eda signaling is necessary for the development and patterning of epithelial placodes of many integumentary organs in both the mouse and chick [19]–[22].”
From Zebrafish eda and edar Mutants Reveal Conserved and Ancestral Roles of Ectodysplasin Signaling in Vertebrates (2008) · cites this paper as [22]
The Introduction says the Eda pathway is required to initiate primary hair follicles in mice, and the Discussion reports that suppressing related signaling in chick skin impairs feather placode formation and changes bud density. But the Discussion also says receptor activity is not required for the initial assumption of placodal fate. The paper does not establish necessity for the placodes of many organ types in both species; these passages have no page number in our copy. (LLM, conf=0.87)
Experimental — accuracy not yet measuredExpression of Eda and Edar is found predominantly in basal epidermal cells, but in feathers Eda is detected in the subjacent mesenchyme as well.
“Expression of Eda and Edar is found predominantly in the basal epidermal cells, but in the case of feathers Eda is detected in the subjacent mesenchyme as well [21],[22].”
From Zebrafish eda and edar Mutants Reveal Conserved and Ancestral Roles of Ectodysplasin Signaling in Vertebrates (2008) · cites this paper as [22]
In “Cloning and expression of the chicken Edar subfamily” (page unavailable), cEdar is detected specifically in the epidermis. “Eda splice variants and protein solubilization” (page unavailable) detects Eda in both epidermis and dermis, supporting the feather-specific dermal component. The paper does not locate either gene specifically in basal epidermal cells; it reports higher Eda transcript levels in the dermis than in the epidermis at E7 and E10, contrary to the claim that Eda is predominantly epidermal. (LLM, conf=0.88)
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Cites
Molecular Mechanisms Regulating Hair Follicle Development
Millar, S. E. (2002) · Journal of Investigative Dermatology · doi:10.1046/j.0022-202x.2001.01670.x · Cited by 967 · see citing works
Kere, J., Srivastava, A. K., Montonen, O., Zonana, J., Thomas, N., Ferguson, B., Munoz, F., Morgan, D., Clarke, A., Baybayan, P., et al. (1996) · Nature Genetics · doi:10.1038/ng0895-409 · Cited by 749 · see citing works
Gene defect in ectodermal dysplasia implicates a death domain adapter in development
Headon, D. J., Emmal, S. A., Ferguson, B. M., Tucker, A. S., Justice, M. J., Sharpe, P. T., Zonana, J., & Overbeek, P. A. (2001) · Nature · doi:10.1038/414913a · Cited by 378 · see citing works
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Research works printed but not linked: 2
- Mou, C., Jackson, B., Schneider, P., Overbeek, P.A., Headon, D.J., 2006. Generation of the primary hair follicle pattern. Proc. Natl. Acad. Sci. U. S. A. 103, 9075-9080.
- Srivastava, A.K., Pispa, J., Hartung, A.J., Du, Y., Ezer, S., Jenks, T., Shimada, T., Pekkanen, M., Mikkola, M.L., Ko, M.S., Thesleff, I., Kere, J., Schlessinger, D., 1997. The Tabby phenotype is caused by mutation in a mouse homologue of the EDA gene that reveals novel mouse and human exons and encodes a protein (ectodysplasin-A) with collagenous domains. Proc. Natl. Acad. Sci. U. S. A. 94, 13069-13074.
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Harris, M. P., Rohner, N., Schwarz, H., Perathoner, S., Konstantinidis, P., & Nüsslein-Volhard, C. (2008) · PLoS Genetics · doi:10.1371/journal.pgen.1000206 · Cited by 224 · see citing works
Development, regeneration, and evolution of feathers
Chen, C.-F., Foley, J., Tang, P.-C., Li, A., Jiang, T. X., Wu, P., Widelitz, R. B., & Chuong, C. M. (2015) · Annual Review of Animal Biosciences · doi:10.1146/annurev-animal-022513-114127 · Cited by 163 · see citing works
Self-citation
- Authors
- Drew, C. F., Lin, C. M., Jiang, T. X., Blunt, G., Mou, C., Chuong, C. M., & Headon, D. J.
- Affiliations
- University of Manchester (GB)
- University of Southern California (US)
- Corresponding author
- Headon, Denis J.
- Venue
- Developmental Biology
- Publisher
- Elsevier BV
- Published
- 2007-05
- Volume
- 305
- Issue
- 1
- Pages
- 232-245
- ISSN
- 0012-1606 (ISSN-L)
- PMC
- PMC2696204
- OpenAlex
- W2151527805
- Cited by
- 59
- References
- 3
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 3 · 2023: 4 · 2021: 3 · 2020: 4 · 2019: 4 · 2018: 3 · 2017: 4 · 2016: 2 · 2015: 2 · 2014: 4 · 2013: 5 · 2012: 3
- FWCI
- 5.87
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 2269 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Developmental Biology (publishedVersion)
- PubMed (publishedVersion)
- Research Explorer (The University of Manchester) (publishedVersion)
- PubMed Central (acceptedVersion)
- Edinburgh Research Explorer (University of Edinburgh) (submittedVersion, other-oa)
- Funders
- National Institutes of Health
- Biotechnology and Biological Sciences Research Council (BBS/B/12083)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR 042177, R01AR042177, AR047364, R01AR047364)
- Topics
- Health Sciences › Medicine › Urology › Hair Growth and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › dental development and anomalies
- Keywords
- EDAR, Troy, TNF receptor superfamily, chickens, NF-κB signaling, death domain, dominant negative receptor
- MeSH terms
- Amino Acid Sequence, Animals, Base Sequence, Chickens, Feathers, Molecular Sequence Data, Morphogenesis, Oligonucleotides, Species Specificity, Blotting, Western, Signal Transduction, NF-kappa B, Conserved Sequence, In Situ Hybridization, Sequence Analysis, DNA, Reverse Transcriptase Polymerase Chain Reaction, Edar-Associated Death Domain Protein
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