Implications for tooth development on ENU-induced ectodermal dysplasia mice

Yeun Jung Kim, Jae Young Kim, Jae Woo Cho, Dal Sun Cha, Min Jung Lee, Tadokoro Osamu, Hyuk Jae Kwon, Kyu Hyuk Cho, Joon H. Lee, Chang Woo Song, Han Sung Jung

Research output: Contribution to journalArticle

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.

Original languageEnglish
Pages (from-to)97-103
Number of pages7
JournalBirth Defects Research Part B - Developmental and Reproductive Toxicology
Volume83
Issue number2
DOIs
Publication statusPublished - 2008 Apr 1

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Ethylnitrosourea
Ectodermal Dysplasia
Tooth
Genes
Phenotype
Mutagens
Chromosomes
Chromosomes, Human, Pair 3
Organogenesis
Osteogenesis
Screening
Bone
Hair
Embryonic Development
Real-Time Polymerase Chain Reaction
Immunohistochemistry
Defects
Genome
Molecules
Staining and Labeling

All Science Journal Classification (ASJC) codes

  • Embryology
  • Toxicology
  • Developmental Biology
  • Health, Toxicology and Mutagenesis

Cite this

Kim, Yeun Jung ; Kim, Jae Young ; Cho, Jae Woo ; Cha, Dal Sun ; Lee, Min Jung ; Osamu, Tadokoro ; Kwon, Hyuk Jae ; Cho, Kyu Hyuk ; Lee, Joon H. ; Song, Chang Woo ; Jung, Han Sung. / Implications for tooth development on ENU-induced ectodermal dysplasia mice. In: Birth Defects Research Part B - Developmental and Reproductive Toxicology. 2008 ; Vol. 83, No. 2. pp. 97-103.
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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.",
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Kim, YJ, Kim, JY, Cho, JW, Cha, DS, Lee, MJ, Osamu, T, Kwon, HJ, Cho, KH, Lee, JH, Song, CW & Jung, HS 2008, 'Implications for tooth development on ENU-induced ectodermal dysplasia mice', Birth Defects Research Part B - Developmental and Reproductive Toxicology, vol. 83, no. 2, pp. 97-103. https://doi.org/10.1002/bdrb.20146

Implications for tooth development on ENU-induced ectodermal dysplasia mice. / Kim, Yeun Jung; Kim, Jae Young; Cho, Jae Woo; Cha, Dal Sun; Lee, Min Jung; Osamu, Tadokoro; Kwon, Hyuk Jae; Cho, Kyu Hyuk; Lee, Joon H.; Song, Chang Woo; Jung, Han Sung.

In: Birth Defects Research Part B - Developmental and Reproductive Toxicology, Vol. 83, No. 2, 01.04.2008, p. 97-103.

Research output: Contribution to journalArticle

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AU - Kim, Yeun Jung

AU - Kim, Jae Young

AU - Cho, Jae Woo

AU - Cha, Dal Sun

AU - Lee, Min Jung

AU - Osamu, Tadokoro

AU - Kwon, Hyuk Jae

AU - Cho, Kyu Hyuk

AU - Lee, Joon H.

AU - Song, Chang Woo

AU - Jung, Han Sung

PY - 2008/4/1

Y1 - 2008/4/1

N2 - 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.

AB - 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.

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