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Stem cell factor rescues tyrosinase expression and pigmentation in discreet anatomic locations in albino mice
Author(s) -
Vanover Jillian C,
Spry Malinda L,
Hamilton Laura,
Wakamatsu Kazumasa,
Ito Shosuke,
D’Orazio John A
Publication year - 2009
Publication title -
pigment cell and melanoma research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.618
H-Index - 105
eISSN - 1755-148X
pISSN - 1755-1471
DOI - 10.1111/j.1755-148x.2009.00617.x
Subject(s) - tyrosinase , melanocyte , stem cell factor , mutant , biology , transgene , melanocortin 1 receptor , microbiology and biotechnology , genetically modified mouse , epidermis (zoology) , melanin , stem cell , genetics , gene , biochemistry , anatomy , enzyme , phenotype , melanoma , progenitor cell
Summary The K14‐SCF transgenic murine model of variant pigmentation is based on epidermal expression of stem cell factor (SCF) on the C57BL/6J background. In this system, constitutive expression of SCF by epidermal keratinocytes results in retention of melanocytes in the interfollicular basal layer and pigmentation of the epidermis itself. Here, we extend this animal model by developing a compound mutant transgenic amelanotic animal defective at both the melanocortin 1 receptor ( Mc1r ) and tyrosinase ( Tyr ) loci. In the presence of K14‐Scf , tyrosinase‐mutant animals (previously thought incapable of synthesizing melanin) exhibited progressive robust epidermal pigmentation with age in the ears and tails. Furthermore, K14‐SCF Tyr c2j/c2j animals demonstrated tyrosinase expression and enzymatic activity, suggesting that the c2j Tyr defect can be rescued in part by SCF in the ears and tail. Lastly, UV sensitivity of K14‐Scf congenic animals depended mainly on the amount of eumelanin present in the skin. These findings suggest that c‐kit signaling can overcome the c2j Tyr mutation in the ears and tails of aging animals and that UV resistance depends on accumulation of epidermal eumelanin.