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This version published online on November 24, 2004
Endocrinology, doi:10.1210/en.2004-0733
A more recent version of this article appeared on March 1, 2005
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Submitted on June 8, 2004
Accepted on November 19, 2004

Preservation of eumelanin hair pigmentation in proopiomelanocortin-deficient mice on a non-agouti (a/a) genetic background

Andrzej Slominski, Przemyslaw M. Plonka, Alexander Pisarchik, James L. Smart, Virginie Tolle, Jacobo Wortsman, and Malcolm J. Low*

Department of Pathology and Laboratory Medicine, University of Tennessee, Memphis, TN 38163, USA; Department of Biophysics, Faculty of Biotechnology, Jagiellonian University, Krakow, Poland; Vollum Institute, Department of Behavioral Neuroscience, and Center for the Study of Weight Regulation and Associated Disorders, Oregon Health & Science University, Portland, OR, 97239, USA; Department of Medicine, Southern Illinois University, Springfield, IL 62704, USA

* To whom correspondence should be addressed. E-mail: low{at}ohsu.edu.

The original strain of proopiomelanocortin (POMC)-deficient mice (Pomc-/-) was generated by homologous recombination in 129 x 1/SvJ (Aw/Aw) derived embryonic stem cells using a targeting construct that deleted exon 3, encoding all the known functional POMC-derived peptides including {alpha}-MSH, from the Pomc gene. While these Pomc-/- mice exhibited adrenal hypoplasia and obesity similar to the syndrome of POMC deficiency in children, their agouti coat color was only subtly altered. To further investigate the mechanism of hair pigmentation in the absence of POMC peptides we studied wild-type (Pomc+/+), heterozygous (Pomc+/-), and homozygous (Pomc-/-) mice on a non-agouti (a/a) 129.B6 hybrid genetic background. All three genotypes had similar black fur pigmentation with yellow hairs behind the ears, around the nipples, and in the perianal area characteristic of inbred C57BL/6 mice. Histologic and electron paramagnetic resonance spectrometry examination demonstrated that hair follicles in back skin of Pomc-/- mice developed with normal structure and eumelanin pigmentation; corresponding molecular analyses however excluded local production of {alpha}-MSH and ACTH, since neither Pomc nor putative Pomc pseudogene mRNAs were detected in the skin. Thus, 129.B6 Pomc null mutant mice produce abundant eumelanin hair pigmentation in spite of their congenital absence of melanocortin ligands. These results suggest that either the mouse melanocortin receptor 1 has sufficient basal activity to trigger and sustain eumelanogenesis in vivo, or that redundant non melanocortin pathway(s) compensate for the melanocortin deficiency. While the latter implies feedback control of melanogenesis, it is also possible that the two mechanisms operate jointly in hair follicles.
Key words: proopiomelanocortin (POMC) • melanocyte-stimulating hormone (MSH) • MC1 receptor • eumelanin • hair pigmentation • targeted gene mutation • mouse skin




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