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Spontaneous melanocytosis in transgenic mice
1Department of Chemical Biology, Laboratory for Cancer Research, College of Pharmacy, Rutgers University, Piscataway, New Jersey 08855, USA.
The Journal of Investigative Dermatology
|May 1, 1996
Summary
A cloned DNA fragment (Clone B) that promotes fat cell differentiation unexpectedly caused melanocytosis in transgenic mice. This study details the melanin lesions and elevated tyrosinase activity, suggesting a model for studying melanin tumors.
Area of Science:
- Genetics and Molecular Biology
- Dermatology
- Oncology
Background:
- Clone B, a 2-kb genomic DNA fragment, is known to induce adipocyte differentiation in vitro.
- Transgenic mice were created using Clone B DNA to study its in vivo effects.
Purpose of the Study:
- To characterize the unexpected phenotype of spontaneous melanocytosis in Clone B transgenic mice.
- To investigate the distribution, morphology, and cellular basis of melanin-containing lesions.
- To explore the potential of these mice as a model for melanin-related tumor research.
Main Methods:
- Generation of transgenic mice carrying the Clone B DNA fragment.
- Gross and microscopic examination of melanin-containing lesions.
- Ultrastructural analysis of affected tissues (dermal lesions, lymph nodes, spleen).
- Protein gel electrophoresis to assess tyrosinase activity.
Main Results:
- Transgenic mice developed spontaneous dermal melanin lesions on ears, snout, and perianal regions by 3-4 months of age.
- Lesions appeared as multifocal dermal masses that spread to adjacent skin.
- Ultrastructural analysis revealed melanin within cells, with organelle effacement in severely affected cells.
- Elevated tyrosinase activity was detected in affected tissues, including skin, lymph nodes, and lesions.
Conclusions:
- The Clone B DNA fragment induces not only adipocyte differentiation but also spontaneous melanocytosis in vivo.
- These transgenic mice exhibit characteristics of melanin-containing tumors, including elevated tyrosinase.
- This mouse model offers a valuable platform for studying the pathogenesis of benign and malignant melanin tumors.