Implications for tooth development on ENU-induced ectodermal dysplasia mice.
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.
Kim
Yeun-Jung
YJ
Division in Anatomy and Developmental Biology, Department of Oral Biology, Research Center for Orofacial Hard Tissue Regeneration, College of Dentistry, Yonsei University, Seoul, Korea.
Kim
Jae-Young
JY
Cho
Jae-Woo
JW
Cha
Dal-Sun
DS
Lee
Min-Jung
MJ
Osamu
Tadokoro
T
Kwon
Hyuk-Jae
HJ
Cho
Kyu-Hyuk
KH
Lee
Joon H
JH
Song
Chang-Woo
CW
Jung
Han-Sung
HS
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
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