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Characterization of melanocyte‐specific inducible Cre recombinase transgenic mice
Author(s) -
Bosenberg Marcus,
Muthusamy Viswanathan,
Curley David P.,
Wang Zhenxiong,
Hobbs Cara,
Nelson Betsy,
Nogueira Cristina,
Horner James W.,
DePinho Ronald,
Chin Lynda
Publication year - 2006
Publication title -
genesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.093
H-Index - 110
eISSN - 1526-968X
pISSN - 1526-954X
DOI - 10.1002/dvg.20205
Subject(s) - melanocyte , cre recombinase , biology , transgene , genetically modified mouse , embryonic stem cell , microbiology and biotechnology , melanocortin 1 receptor , melanoma , genetics , phenotype , gene
Conditional Cre‐mediated recombination has emerged as a robust method of introducing somatic genetic alterations in an organ‐specific manner in the mouse. Here, we generated and characterized mice harboring a 4‐hydroxytamoxifen (OHT)‐inducible Cre recombinase‐estrogen receptor fusion transgene under the control of the melanocyte‐specific tyrosinase promoter, designated Tyr::CreER T2 . Cre‐mediated recombination was induced in melanocytes in a spatially and temporally controlled manner upon administration of OHT and was documented in embryonic melanoblasts, follicular bulb melanocytes, dermal dendritic melanocytes, epidermal melanocytes of tail skin, and in putative melanocyte stem cells located within the follicular bulge. Functional evidence suggestive of recombination in follicular melanocyte stem cells included the presence of Cre‐mediated recombination in follicular bulb melanocytes 1 year after topical OHT administration, by which time several hair cycles have elapsed and the melanocytes residing in this location have undergone multiple rounds of apoptosis and replenishment. These Tyr:: CreER T2 transgenic mice represent a useful resource for the evaluation of melanocyte developmental genetics, the characterization of melanocyte stem cell function and dynamics, and the construction of refined mouse models of malignant melanoma. genesis 44:262–267, 2006. Published 2006 Wiley‐Liss, Inc.