International Mammalian Genome Society

17th International Mouse Genome Conference

9-12 November 2003, Braunschweig, Germany

Plenary Presentations * Oral Presentations *
Poster Presentations: Behavioural Genetics and Genomics * Development and Stem Cells * Functional Genome Analysis * Mouse Models of Human Disease * Mouse System Biology Bioinformatics * Multigenic and Multifactorial Trait Analysis * Nutrition and Metabolic Disease * Phenotyping Methods Imaging * The Genetics and Genomics of Infectious Disease *
Verne Chapman Memorial Lecture * Table of Contents * Sponsor/Exhibitor List * Awards * Photographs

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POSTER 81 - DEVELOPMENT OF SKIN AND HAIR-RELATED DEFECT MICE DERIVED ENU-MUTAGENESIS

Cho KH
Korea Institute of Toxicology(KIT), Korea Research Institute chemical of Toxicology(KRICT)

Co-Authors: Nam Y Y, Cho J W, Song C W, Han S S
Institutions: Korea Institute of Toxicology(KIT), Korea Research Institute chemical of Toxicology(KRICT)

ENU mutagenesis screening has developed many novel and allelic mutant mice. We could already screen 63 dominant and recessive mutations. In this study, pathological analysis and chromosome localization were carried out about the mutant with hair and skin defect.

Microgenia: The mutant mouse exhibited no teeth, the lack of lipid layer in dermis, abnormal hair follicle cycle and parakeratosis, and early death within 21 days old. It could be distinguished from normal littermates at 14-15 embryonic day because it began to have a snout anomaly at that time. Its responsible gene was located on Chr 3.

Nude-like: It exhibited total alopecia, wrinkled skin and long curved nails. This mutant was inherited by an autosomal recessive mode. The causative gene was linked to D14Mit193 near hr gene on chromosome 14. Affected skin developed deep dermal cysts, and decreased number of hair follicle. This mutant might be used as an important model for human disease as papular atrichia.

Hair poor: It had poor and short hair of whole body. Abnormal hair cycle and decreased number of vibrissae were characteristic. Its genetic mode was semi dominant. When it was homozygote, total alopecia occurred and anomaly of mutant hair follicle structure was more severe than that of the normal.

Lamb wool: It had dysmorphology of hair structure and length. The hair was long and curly. Mutants began to be distinguished from normal littermates at 7~10 days old. The causative gene was transferred to next generation by autosomal recessive mode.