Involvement of a novel Tnf receptor homologue in hair follicle induction.
Abstract
Although inductive interactions are known to be essential for specification of cell fate in many vertebrate tissues, the signals and receptors responsible for transmitting this information remain largely unidentified. Mice with mutations in the downless (dl) gene have defects in hair follicle induction, lack sweat glands and have malformed teeth. These structures originate as ectodermal placodes, which invaginate into the underlying mesenchyme and differentiate to form specific organs. Positional cloning of the dl gene began with identification of the transgenic family OVE1. One branch of the family, dl(OVE1B), carries an approximately 600-kb deletion at the dl locus caused by transgene integration. The mutated locus has been physically mapped in this family, and a 200-kb mouse YAC clone, YAC D9, has been identified and shown to rescue the dl phenotype in the spontaneous dl(Jackson) (dl(J), recessive) and Dl(sleek) (Dl(slk), dominant negative) mutants. Here we report the positional cloning of the dl gene, which encodes a novel member of the tumour necrosis factor (Tnf) receptor (Tnfr) family. The mutant phenotype and dl expression pattern suggests that this gene encodes a receptor that specifies hair follicle fate. Its ligand is likely to be the product of the tabby (Ta) gene, as Ta mutants have a phenotype identical to that of dl mutants and Ta encodes a Tnf-like protein.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The downless mouse mutant, which has a mutation that disrupts the mouse Edar gene, causes arrest of placode formation at a pre-placode stage of development (P0-P1).
“They report that the downless mouse mutant, which has a mutation that disrupts the mouse Edar gene [36], causes arrest of placode formation at a pre-placode stage of development (P0–P1).”
From Zebrafish eda and edar Mutants Reveal Conserved and Ancestral Roles of Ectodysplasin Signaling in Vertebrates (2008) · cites this paper as [36]
Cites
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
Flagged first, then by citations
Cited by
Sorted by citations
The TNF and TNF Receptor Superfamilies
Locksley, R. M., Killeen, N., & Lenardo, M. J. (2001) · Cell · doi:10.1016/s0092-8674(01)00237-9 · Cited by 3,650 · see citing works
WNT Signals Are Required for the Initiation of Hair Follicle Development
Andl, T., Reddy, S. T., Gaddapara, T., & Millar, S. E. (2002) · Developmental Cell · doi:10.1016/s1534-5807(02)00167-3 · Cited by 1,088 · see citing works
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
Zonana, J., Elder, M. E., Schneider, L. C., Orlow, S. J., Moss, C., Golabi, M., Shapira, S. K., Farndon, P. A., Wara, D. W., Emmal, S. A., et al. (2000) · The American Journal of Human Genetics · doi:10.1086/316914 · Cited by 521 · see citing works
Monreal, A. W., Ferguson, B. M., Headon, D. J., Street, S. L., Overbeek, P. A., & Zonana, J. (1999) · Nature Genetics · doi:10.1038/11937 · Cited by 397 · see citing works
Self-citationGene 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
Self-citationDepew, M. J., Tucker, A. S., & Sharpe, P. T. (2002) · Mouse Development · doi:10.1016/b978-012597951-1/50023-8 · Cited by 259 · see citing works
Chen, D., Jarrell, A., Guo, C., Lang, R., & Atit, R. (2012) · Development · doi:10.1242/dev.076463 · Cited by 260 · see citing works
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
Richardson, G. D., Bazzi, H., Fantauzzo, K. A., Waters, J. M., Crawford, H., Hynd, P., Christiano, A. M., & Jahoda, C. A. B. (2009) · Development · doi:10.1242/dev.031427 · Cited by 103 · see citing works
Epidermal patterning and induction of different hair types during mouse embryonic development
Duverger, O., & Morasso, M. I. (2009) · Birth Defects Research Part C: Embryo Today: Reviews · doi:10.1002/bdrc.20158 · Cited by 102 · see citing works
Ectodysplasin A (EDA) – EDA receptor signalling and its pharmacological modulation
Kowalczyk-Quintas, C., & Schneider, P. (2014) · Cytokine & Growth Factor Reviews · doi:10.1016/j.cytogfr.2014.01.004 · Cited by 97 · see citing works
Autosomal dominant anhidrotic ectodermal dysplasias at the EDARADD locus
Bal, E., Baala, L., Cluzeau, C., El Kerch, F., Ouldim, K., Hadj-Rabia, S., Bodemer, C., Munnich, A., Courtois, G., Sefiani, A., et al. (2007) · Human Mutation · doi:10.1002/humu.20500 · Cited by 100 · see citing works
- Authors
- Headon, D. J., & Overbeek, P. A.
- Affiliations
- Baylor College of Medicine (US)
- Corresponding author
- Overbeek, Paul A.
- Venue
- Nature Genetics
- Published
- 1999-08
- Volume
- 22
- Issue
- 4
- Pages
- 370-374
- ISSN
- 1061-4036 (ISSN-L)
- 1546-1718
- OpenAlex
- W1548753322
- Cited by
- 379
- References
- 1
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 4 · 2023: 15 · 2022: 14 · 2021: 10 · 2020: 8 · 2019: 12 · 2018: 10 · 2017: 9 · 2016: 8 · 2015: 7 · 2014: 12 · 2013: 9 · 2012: 13
- FWCI
- 28.84
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Genetics (publishedVersion)
- PubMed (publishedVersion)
- Research Explorer (The University of Manchester) (publishedVersion)
- Funders
- National Heart, Lung, and Blood Institute (HL49953, P01HL049953)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR045316, AR45316)
- Topics
- Health Sciences › Medicine › Urology › Hair Growth and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › dental development and anomalies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Keywords
- hair follicle induction, positional cloning, cell fate specification, sweat gland development, tooth development, dominant-negative mutant, transgenic mice
- MeSH terms
- Amino Acid Sequence, Animals, Cloning, Molecular, Humans, Membrane Proteins, Models, Genetic, Molecular Sequence Data, Phenotype, Proteins, Skin, Trans-Activators, Sequence Homology, Amino Acid, Receptors, Tumor Necrosis Factor, Hair Follicle, Bone Morphogenetic Proteins, Mice, Ectodysplasins, Receptors, Ectodysplasin, Edar Receptor, Hedgehog Proteins, Bone Morphogenetic Protein 4
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
