Agouti-signaling protein is a protein that in humans is encoded by the ASIP gene.[5][6] It is responsible for the distribution of melanin pigment in mammals.[7][8] Agouti interacts with the melanocortin 1 receptor to determine whether the melanocyte (pigment cell) produces phaeomelanin (a red to yellow pigment), or eumelanin (a brown to black pigment).[9] This interaction is responsible for making distinct light and dark bands in the hairs of animals such as the agouti, which the gene is named after. In other species such as horses, agouti signalling is responsible for determining which parts of the body will be red or black. Mice with wildtype agouti will be grey-brown, with each hair being partly yellow and partly black. Loss of function mutations in mice and other species cause black fur coloration, while mutations causing expression throughout the whole body in mice cause yellow fur and obesity.[10]
The agouti-signaling protein (ASIP) is a competitive antagonist with alpha-Melanocyte-stimulating hormone (α-MSH) to bind with melanocortin 1 receptor (MC1R) proteins. Activation by α-MSH causes production of the darker eumelanin, while activation by ASIP causes production of the redder phaeomelanin.[11] This means where and while agouti is being expressed, the part of the hair that is growing will come out yellow rather than black.
^Wilson BD, Ollmann MM, Kang L, Stoffel M, Bell GI, Barsh GS (February 1995). "Structure and function of ASP, the human homolog of the mouse agouti gene". Human Molecular Genetics. 4 (2): 223–30. doi:10.1093/hmg/4.2.223. PMID7757071.
^Silvers WK, Russell ES (1955). "An experimental approach to action of genes at the agouti locus in the mouse". Journal of Experimental Zoology. 130 (2): 199–220. Bibcode:1955JEZ...130..199S. doi:10.1002/jez.1401300203.
^Millar SE, Miller MW, Stevens ME, Barsh GS (October 1995). "Expression and transgenic studies of the mouse agouti gene provide insight into the mechanisms by which mammalian coat color patterns are generated". Development. 121 (10): 3223–32. doi:10.1242/dev.121.10.3223. PMID7588057.