title: Implications for tooth development on ENU-induced ectodermal dysplasia mice.
abstract: BACKGROUND
  In this study, the mutated phenotypes were produced by treatment of chemical mutagen, N-ethyl-N-nitrosourea (ENU). We analyzed the mutated mice showing the specific phenotype of ectodermal dysplasia (ED) and examined the affected gene.
  
  
  METHODS
  Phenotypes, including size, bone formation, and craniofacial morphology of ENU-induced ED mice, were focused. Tooth development and expression of several molecules were analyzed by histologic observations and immunohistochemistry. We carried out genome-wide screening and quantitative real-time PCR to define the affected and related genes.
  
  
  RESULTS
  As examined previously in human ectodermal dysplasia, ENU-induced ED mice showed the specific morphologic deformities in tooth, hair, and craniofacial growth. Tooth development in the ENU-induced ED mice ceased at early cap stage. In addition, skeletal staining showed retardation in craniofacial development. Finally, the affected gene, which would be involved in the mechanism of ED, was located between the marker D3Mit14 and D3Mit319 on chromosome 3.
  
  
  CONCLUSIONS
  The affected gene in ENU-induced ED mice showed several defects in ectodermal organogenesis and these results indicate that this gene plays an important role in mouse embryogenesis.
authors: Division in Anatomy and Developmental Biology, Department of Oral Biology, Research Center for Orofacial Hard Tissue Regeneration, College of Dentistry, Yonsei University, Seoul, Korea.
authors: Yeun-Jung
authors: YJ
authors: Kim
authors: Jae-Young
authors: JY
authors: Kim
authors: Jae-Woo
authors: JW
authors: Cho
authors: Dal-Sun
authors: DS
authors: Cha
authors: Min-Jung
authors: MJ
authors: Lee
authors: Tadokoro
authors: T
authors: Osamu
authors: Hyuk-Jae
authors: HJ
authors: Kwon
authors: Kyu-Hyuk
authors: KH
authors: Cho
authors: Joon H
authors: JH
authors: Lee
authors: Chang-Woo
authors: CW
authors: Song
authors: Han-Sung
authors: HS
authors: Jung
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D002874:Chromosome Mapping; D033481:Chromosomes, Mammalian; D004476:Ectodermal Dysplasia / Q000139:chemically induced* / Q000196:embryology / Q000235:genetics; D053331:Ectodysplasins / Q000235:genetics / Q000378:metabolism; D005038:Ethylnitrosourea / Q000633:toxicity*; D005260:Female; D018507:Gene Expression Regulation, Developmental / Q000187:drug effects; D028322:Inhibin-beta Subunits / Q000235:genetics; D036341:Intercellular Signaling Peptides and Proteins / Q000235:genetics; D051821:Lymphoid Enhancer-Binding Factor 1 / Q000235:genetics; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D038081:Organogenesis / Q000187:drug effects; D015398:Signal Transduction / Q000235:genetics; D014071:Tooth Abnormalities / Q000139:chemically induced* / Q000196:embryology / Q000235:genetics; D051996:Transcription Factor RelA / Q000235:genetics
chemical_list: C405060:Dkk2 protein, mouse; D053331:Ectodysplasins; C506019:Eda protein, mouse; D036341:Intercellular Signaling Peptides and Proteins; C497574:Lef1 protein, mouse; D051821:Lymphoid Enhancer-Binding Factor 1; D051996:Transcription Factor RelA; C103008:inhibin beta A subunit; D028322:Inhibin-beta Subunits; D005038:Ethylnitrosourea