A biochemical function for attractin in agouti-induced pigmentation and obesity

Lin He, Teresa M. Gunn, Donna M. Bouley, Xin Yun Lu, Stanley J. Watson, Stuart F. Schlossman, Jonathan S. Duke-Cohan, Gregory S. Barsh

Research output: Contribution to journalArticle

111 Scopus citations

Abstract

Agouti protein, a paracrine signaling molecule normally limited to skin, is ectopically expressed in lethal yellow (Aγ) mice, and causes obesity by mimicking agouti-related protein (Agrp), found primarily in the hypothalamus. Mouse attractin (Atrn) is a widely expressed transmembrane protein whose loss of function in mahogany (Atrnmg-3J/Atrnmg-3J) mutant mice blocks the pleiotropic effects of Aγ. Here we demonstrate in transgenic, biochemical and genetic-interaction experiments that attractin is a low-affinity receptor for agouti protein, but not Agrp, in vitro and in vivo. Additional histopathologic abnormalities in Atrnmg-3J/Atrnmg-3J mice and cross-species genomic comparisons indicate that Atrn has multiple functions distinct from both a physiologic and an evolutionary perspective.

Original languageEnglish (US)
Pages (from-to)40-47
Number of pages8
JournalNature Genetics
Volume27
Issue number1
DOIs
StatePublished - Jan 20 2001
Externally publishedYes

ASJC Scopus subject areas

  • Genetics

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    He, L., Gunn, T. M., Bouley, D. M., Lu, X. Y., Watson, S. J., Schlossman, S. F., Duke-Cohan, J. S., & Barsh, G. S. (2001). A biochemical function for attractin in agouti-induced pigmentation and obesity. Nature Genetics, 27(1), 40-47. https://doi.org/10.1038/83741