How is coat color inherited in mice? - briefly
Coat pigmentation in mice follows Mendelian patterns, with alleles at loci such as Agouti, Albino, and Dilute controlling the synthesis of eumelanin or pheomelanin. Dominant alleles generate darker fur, whereas recessive mutations result in lighter or albino phenotypes.
How is coat color inherited in mice? - in detail
Mouse coat coloration is transmitted through a set of autosomal loci that follow classic Mendelian dominance, with several loci exerting epistatic control over others. The primary loci are:
- Agouti (A) – dominant allele produces banded hairs (agouti pattern); recessive a yields solid eumelanin (black or brown).
- Extension (E) – dominant E permits eumelanin synthesis; recessive e restricts pigment to phaeomelanin, giving yellow or red coats.
- Black (B) – dominant B results in black eumelanin; recessive b converts eumelanin to brown.
- Dilute (d) – dominant D yields full pigment intensity; recessive d lightens black to gray and brown to chocolate.
- Albino (c) – recessive homozygote c/c eliminates melanin production, producing a completely white mouse and masking all other color genes.
- White spotting (S) – dominant S creates patches of unpigmented skin; homozygous S/S can produce extensive spotting or near‑total white.
These loci interact hierarchically. For example, a mouse homozygous for the albino allele (c/c) will appear white regardless of its A, B, or E genotype, because melanin synthesis is blocked. Similarly, the presence of the dominant white‑spotting allele can overlay any underlying coloration with unpigmented areas.
Molecularly, the A locus corresponds to the agouti signaling protein (ASIP), which antagonizes the melanocortin‑1 receptor (MC1R) encoded by the E locus. When ASIP is active, MC1R signaling is reduced, leading to phaeomelanin deposition. Loss of ASIP function (a allele) allows continuous MC1R activity and uniform eumelanin production. Mutations in the Tyrosinase (Tyr) gene generate the c allele, abolishing melanin synthesis.
Typical breeding outcomes illustrate the inheritance patterns. Crossing an agouti, black mouse (A/B; E/E; c+/c+) with a non‑agouti, brown mouse (a/a; e/e; c+/c+) yields F1 progeny that are heterozygous at each locus (A/a; B/b; E/e). Phenotypically, these F1 individuals display agouti black because A and E are dominant. A subsequent intercross of F1s produces a 9:3:3:1 phenotypic ratio for agouti black : agouti brown : non‑agouti black : non‑agouti brown, assuming independent assortment of the A, B, and E loci.
Modifiers and quantitative trait loci further refine hue, intensity, and pattern. The dilute locus (d) reduces pigment saturation, while additional genes influence tail tip color, eye pigmentation, and the extent of white spotting.
Because coat color genes are autosomal and readily observable, they serve as convenient genetic markers in laboratory mouse strains, allowing rapid verification of genotype inheritance, assessment of linkage, and tracking of introgressed alleles across breeding programs.