[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.

Pleiotropic effects of constitutive expression of the mouse gene include adult-onset obesity, increased tumor susceptibility, and premature infertility.

[15][16] Agouti is not directly secreted in the melanocyte as it works as a paracrine factor on dermal papillae cells to inhibit release of melanocortin.

[17] Melanocortin acts on follicular melanocytes to increase production of eumelanin, a melanin pigment responsible for brown and black hair.

When agouti is expressed, production of pheomelanin dominates, a melanin pigment that produces yellow or red colored hair.

This deletion causes the genomic sequence of agouti to be lost, except the promoter and the first non-encoding exon of Raly, a ubiquitously expressed gene in mammals.

This is caused by the insertion of a single intracisternal A particle (IAP) retrotransposon upstream to the start site of agouti transcription.

[22] In the proximal end of the gene, an unknown promoter then causes agouti to be constitutionally activated, and individuals to present with phenotypes consistent with the lethal yellow mutation.

Although the mechanism for the activation of the promoter controlling the viable yellow mutation is unknown, the strength of coat color has been correlated with the degree of gene methylation, which is determined by maternal diet and environmental exposure.

[22] Agouti also promotes obesity by antagonizing melanocyte-stimulating hormone (MSH) at the melanocortin receptor (MC4R), as MC4R is responsible for regulating food intake by inhibiting appetite signals.

Methylation occurs in six guanine-cytosine (GC) rich sequences in the 5’ long terminal repeat of the IAP element in the viable yellow mutation.

Low levels of methylation can induce gene imprinting which results in offspring displaying consistent phenotypes to their parents, as ectopic expression of agouti is inherited through non-genomic mechanisms.

Ensuring maternal diets are high in methyl equivalents is a key preventive measure for reducing ectopic expression of agouti in offspring.

If the same mother had eaten a methyl-rich diet supplemented with zinc, vitamin B12, and folic acid then the offspring's agouti gene would likely become methylated, it wouldn't be expressed, and the coat color would be brown instead.

[22] ASP has neuroendocrine functions consistent with murine agouti, as it agonizes via AgRP neurons in the hypothalamus and antagonizes MSH at MC4Rs which reduce satiety signals.

[34][35] The mechanism underlying hyperinsulinemia in humans is consistent with murine agouti, as insulin secretion is heightened through calcium sensitive signaling in pancreatic beta cells.