The mouse mahogany locus encodes a transmembrane form of human attractin

Teresa M. Gunn, Kimberly A. Miller, Lin He, Richard W. Hyman, Ronald W. Davis, Arezou Azarani, Stuart F. Schlossman, Jonathan S. Duke-Cohan and Gregory S. Barsh ()
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Teresa M. Gunn: Stanford University School of Medicine
Kimberly A. Miller: Stanford University School of Medicine
Lin He: Stanford University School of Medicine
Richard W. Hyman: Stanford University School of Medicine
Ronald W. Davis: Stanford University School of Medicine
Arezou Azarani: Stanford University School of Medicine
Stuart F. Schlossman: Dana-Farber Cancer Institute, Harvard Medical School
Jonathan S. Duke-Cohan: Dana-Farber Cancer Institute, Harvard Medical School
Gregory S. Barsh: Stanford University School of Medicine

Nature, 1999, vol. 398, issue 6723, 152-156

Abstract: Abstract Agouti protein and agouti-related protein are homologous paracrine signalling molecules that normally regulate hair colour and body weight, respectively, by antagonizing signalling through melanocortin receptors1,2,3,4,5,6,7. Expression of Agouti is normally limited to the skin, but rare alleles from which Agouti is expressed ubiquitously, such as lethal yellow, have pleiotropic effects that include a yellow coat, obesity, increased linear growth, and immune defects8,9,10,11. The mahogany (mg) mutation suppresses the effects of lethal yellow on pigmentation and body weight, and results of our previous genetic studies place mg downstream of transcription of Agouti but upstream of melanocortin receptors12. Here we use positional cloning to identify a candidate gene for mahogany, Mgca. The predicted protein encoded by Mgca is a 1,428-amino-acid, single-transmembrane-domain protein that is expressed in many tissues, including pigment cells and the hypothalamus. The extracellular domain of the Mgca protein is the orthologue of human attractin, a circulating molecule produced by activated T cells that has been implicated in immune-cell interactions13,14. These observations provide new insight into the regulation of energy metabolism and indicate a molecular basis for crosstalk between melanocortin-receptor signalling and immune function.

Date: 1999
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DOI: 10.1038/18217

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