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J Biol Chem, Vol. 273, Issue 31, 19560-19565, July 31, 1998
From the ¶ Division of Pediatric Hematology/Oncology,
Children's Hospital and Dana Farber Cancer Institute, Harvard Medical
School, Boston, Massachusetts 02115, § St. George's
Hospital Medical School, London SW17 ORE, United Kingdom, and
In mouse follicular melanocytes, production of
eumelanins (brown-black pigments) and pheomelanins (yellow-brownish
pigments) is under the control of two intercellular signaling molecules that exert opposite actions,
Involvement of Microphthalmia in the Inhibition of Melanocyte
Lineage Differentiation and of Melanogenesis by Agouti Signal
Protein
,,,, and
INSERM U385, Biologie et Physiopathologie de la Peau,
Faculté de Médecine, 06107 Nice Cedex 2, France
-melanocyte-stimulating hormone (MSH) which preferentially increases the synthesis of eumelanins, and agouti signal protein (ASP) whose expression favors the production of hair containing pheomelanins. In this study, we report that ASP does
not only affect mature melanocytes but can also inhibit the
differentiation of melanoblasts. We show that both MSH and forskolin
promote the differentiation of murine melanoblasts into mature
melanocytes and that ASP inhibits this process. We present evidence
that the expression of a specific melanogenic transcription factor,
microphthalmia, and its binding to an M box regulatory element, is
inhibited by ASP. We also show that, in B16 murine melanoma cells, ASP
inhibits MSH-stimulated expression of tyrosinase, tyrosine-related
proteins 1 and 2 through an inhibition of the transcription activity of
their respective promoters. Further, ASP inhibits MSH-induced
expression of the microphthalmia gene and reduces the level of
microphthalmia in the cells. Our data demonstrate that ASP can regulate
both melanoblast differentiation and melanogenesis, pointing out the
key role of microphthalmia in the control of these processes.
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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