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Article: Regulation of hair follicle development by the TNF signal ectodysplasin and its receptor Edar

TitleRegulation of hair follicle development by the TNF signal ectodysplasin and its receptor Edar
Authors
Issue Date2002
PublisherThe Company of Biologists Ltd. The Journal's web site is located at http://dev.biologists.org
Citation
Development, 2002, v. 129 n. 10, p. 2541-2553 How to Cite?
AbstractX-linked and autosomal forms of anhidrotic ectodermal dysplasia syndromes (HED) are characterized by deficient development of several ectodermal organs, including hair, teeth and exocrine glands. The recent cloning of the genes that underlie these syndromes, ectodysplasin (ED1) and the ectodysplasin A receptor (EDAR), and their identification as a novel TNF ligand-receptor pair suggested a role for TNF signaling in embryonic morphogenesis. In the mouse, the genes of the spontaneous mutations Tabby (Ta) and downless (dl) were identified as homologs of ED1 and EDAR, respectively. To gain insight into the function of this signaling pathway in development of skin and hair follicles, we analyzed the expression and regulation of Eda and Edar in wild type as well as Tabby and Lef1 mutant mouse embryos. We show that Eda and Edar expression is confined to the ectoderm and occurs in a pattern that suggests a role of ectodysplasin/Edar signaling in the interactions between the ectodermal compartments and the formation and function of hair placodes. By using skin explant cultures, we further show that this signaling pathway is intimately associated with interactions between the epithelial and mesenchymal tissues. We also find that Ta mutants lack completely the placodes of the first developing tylotrich hairs, and that they do not show patterned expression of placodal genes, including Bmp4, Lef1, Shh, Ptch and Edar, and the genes for β-catenin and activin A. Finally, we identified activin as a mesenchymal signal that stimulates Edar expression and WNT as a signal that induces Eda expression, suggesting a hierarchy of distinct signaling pathways in the development of skin and hair follicles. In conclusion, we suggest that Eda and Edar are associated with the onset of ectodermal patterning and that ectodysplasin/edar signaling also regulates the morphogenesis of hair follicles.
Persistent Identifierhttp://hdl.handle.net/10722/169538
ISSN
2015 Impact Factor: 6.059
2015 SCImago Journal Rankings: 5.239
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLaurikkala, Jen_US
dc.contributor.authorPispa, Jen_US
dc.contributor.authorJung, HSen_US
dc.contributor.authorNieminen, Pen_US
dc.contributor.authorMikkola, Men_US
dc.contributor.authorWang, Xen_US
dc.contributor.authorSaarialhoKere, Uen_US
dc.contributor.authorGalceran, Jen_US
dc.contributor.authorGrosschedl, Ren_US
dc.contributor.authorThesleff, Ien_US
dc.date.accessioned2012-10-25T04:52:40Z-
dc.date.available2012-10-25T04:52:40Z-
dc.date.issued2002en_US
dc.identifier.citationDevelopment, 2002, v. 129 n. 10, p. 2541-2553en_US
dc.identifier.issn0950-1991en_US
dc.identifier.urihttp://hdl.handle.net/10722/169538-
dc.description.abstractX-linked and autosomal forms of anhidrotic ectodermal dysplasia syndromes (HED) are characterized by deficient development of several ectodermal organs, including hair, teeth and exocrine glands. The recent cloning of the genes that underlie these syndromes, ectodysplasin (ED1) and the ectodysplasin A receptor (EDAR), and their identification as a novel TNF ligand-receptor pair suggested a role for TNF signaling in embryonic morphogenesis. In the mouse, the genes of the spontaneous mutations Tabby (Ta) and downless (dl) were identified as homologs of ED1 and EDAR, respectively. To gain insight into the function of this signaling pathway in development of skin and hair follicles, we analyzed the expression and regulation of Eda and Edar in wild type as well as Tabby and Lef1 mutant mouse embryos. We show that Eda and Edar expression is confined to the ectoderm and occurs in a pattern that suggests a role of ectodysplasin/Edar signaling in the interactions between the ectodermal compartments and the formation and function of hair placodes. By using skin explant cultures, we further show that this signaling pathway is intimately associated with interactions between the epithelial and mesenchymal tissues. We also find that Ta mutants lack completely the placodes of the first developing tylotrich hairs, and that they do not show patterned expression of placodal genes, including Bmp4, Lef1, Shh, Ptch and Edar, and the genes for β-catenin and activin A. Finally, we identified activin as a mesenchymal signal that stimulates Edar expression and WNT as a signal that induces Eda expression, suggesting a hierarchy of distinct signaling pathways in the development of skin and hair follicles. In conclusion, we suggest that Eda and Edar are associated with the onset of ectodermal patterning and that ectodysplasin/edar signaling also regulates the morphogenesis of hair follicles.en_US
dc.languageengen_US
dc.publisherThe Company of Biologists Ltd. The Journal's web site is located at http://dev.biologists.orgen_US
dc.relation.ispartofDevelopmenten_US
dc.subject.meshActivins - Genetics - Metabolismen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCytoskeletal Proteins - Genetics - Metabolismen_US
dc.subject.meshDna-Binding Proteins - Genetics - Metabolismen_US
dc.subject.meshEctoderm - Metabolismen_US
dc.subject.meshEctodysplasinsen_US
dc.subject.meshEdar Receptoren_US
dc.subject.meshEpidermis - Cytologyen_US
dc.subject.meshFish Proteins - Genetics - Metabolismen_US
dc.subject.meshHair Follicle - Embryology - Metabolismen_US
dc.subject.meshInhibin-Beta Subunits - Genetics - Metabolismen_US
dc.subject.meshLymphoid Enhancer-Binding Factor 1en_US
dc.subject.meshMembrane Proteins - Genetics - Metabolismen_US
dc.subject.meshMesoderm - Metabolismen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Mutant Strainsen_US
dc.subject.meshMutationen_US
dc.subject.meshOrgan Culture Techniquesen_US
dc.subject.meshProto-Oncogene Proteins - Genetics - Metabolismen_US
dc.subject.meshSignal Transductionen_US
dc.subject.meshTrans-Activatorsen_US
dc.subject.meshTranscription Factors - Genetics - Metabolismen_US
dc.subject.meshTumor Necrosis Factor-Alpha - Metabolismen_US
dc.subject.meshWnt Proteinsen_US
dc.subject.meshBeta Cateninen_US
dc.titleRegulation of hair follicle development by the TNF signal ectodysplasin and its receptor Edaren_US
dc.typeArticleen_US
dc.identifier.emailJung, HS: hsjung@yuhs.acen_US
dc.identifier.authorityJung, HS=rp01683en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid11973284-
dc.identifier.scopuseid_2-s2.0-0036333966en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036333966&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume129en_US
dc.identifier.issue10en_US
dc.identifier.spage2541en_US
dc.identifier.epage2553en_US
dc.identifier.isiWOS:000176063600020-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridLaurikkala, J=13604795700en_US
dc.identifier.scopusauthoridPispa, J=24342045800en_US
dc.identifier.scopusauthoridJung, HS=7403030195en_US
dc.identifier.scopusauthoridNieminen, P=7103275437en_US
dc.identifier.scopusauthoridMikkola, M=13606334600en_US
dc.identifier.scopusauthoridWang, X=8767805300en_US
dc.identifier.scopusauthoridSaarialhoKere, U=7006180757en_US
dc.identifier.scopusauthoridGalceran, J=7007033431en_US
dc.identifier.scopusauthoridGrosschedl, R=7007127751en_US
dc.identifier.scopusauthoridThesleff, I=7005319521en_US

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