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Constitutive gray hair in mice induced by melanocyte‐specific deletion of c‐Myc
Author(s) -
Pshenichnaya Irina,
Schouwey Karine,
Armaro Marzia,
Larue Lionel,
Knoepfler Paul S.,
Eisenman Robert N.,
Trumpp Andreas,
Delmas Véronique,
Beermann Friedrich
Publication year - 2012
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.2012.00998.x
Subject(s) - melanocyte , biology , neural crest , phenotype , transgene , genetically modified mouse , microbiology and biotechnology , melanin , microphthalmia associated transcription factor , hair cycle , melanocortin 1 receptor , hair follicle , melanoma , genetics , embryo , transcription factor , gene
Summary c‐Myc is involved in the control of diverse cellular processes and implicated in the maintenance of different tissues including the neural crest. Here, we report that c‐Myc is particularly important for pigment cell development and homeostasis. Targeting c‐Myc specifically in the melanocyte lineage using the floxed allele of c‐Myc and Tyr::Cre transgenic mice results in a congenital gray hair phenotype. The gray coat color is associated with a reduced number of functional melanocytes in the hair bulb and melanocyte stem cells in the hair bulge. Importantly, the gray phenotype does not progress with time, suggesting that maintenance of the melanocyte through the hair cycle does not involve c‐Myc function. In embryos, at E13.5, c‐Myc‐deficient melanocyte precursors are affected in proliferation in concordance with a reduction in numbers, showing that c‐Myc is required for the proper melanocyte development. Interestingly, melanocytes from c‐Myc‐deficient mice display elevated levels of the c‐Myc paralog N‐Myc. Double deletion of c‐Myc and N‐Myc results in nearly complete loss of the residual pigmentation, indicating that N‐Myc is capable of compensating for c‐Myc loss of function in melanocytes.