The dun gene lightens most of the body while leaving the mane, tail, legs, and primitive markings the shade of the undiluted base coat color.
A classic "bay dun" is a gray-gold or tan, characterized by a body color ranging from sandy yellow to reddish brown.
Manes, tails, primitive markings, and other dark areas are usually the shade of the undiluted base coat color.
Zebras can also be considered a variant of dun where the dilution is so extreme it turns the hair nearly white, and the primitive markings (like the striped leg barring) extend across the entire body.
[5] Dun traits include the following: Other variations result from the interplay of additional genes: A single copy of the cream gene on a black base coat does not significantly lighten black hair, though it may have a subtle effect,[8] and thus a single copy generally has no visible effect on a grullo, either.
Thus, if a horse with two cream dilution alleles also carries the dun gene, it also will be cream-colored, with primitive markings not visible to any significant degree.
[10] Historically, before modern genetic studies distinguished between alleles, diluted colors were sometimes lumped together and simply called "dun".
A buckskin is bay horse with the addition of the cream gene, causing the coat color to be diluted from red to gold, usually without primitive markings.
[12] Today, pedigree analysis, DNA testing, studying possible offspring, and the vividness of primitive markings are used to determine whether a horse is a dun.
On such horses, the light-shaded primitive markings are most noticeable during the summer months, when the winter hair sheds.
Countershading such as light dorsal stripes resulting from the presence of the gene nd1 (see section below) may be difficult to detect on light-colored horses.
[4] Genetic analysis and DNA sequencing results published in 2015 link dun color to the T-box 3 (TBX3) transcription factor.
Abnormalities are linked to a collection of developmental defects called ulnar–mammary syndrome, and the null allele (being unable to produce any TBX3 at all) is thought to be embryonic lethal.
[14] In non-dun horses, the TBX3 protein is still functional, and is still produced in most cells, but not expressed in the hair cortex.
The region deleted in non-dun2 is predicted to include binding sites for the transcription factors ALX4 and MSX2, which are both known to be involved in hair follicle development.
This indicates that the hair follicles of dun and non-dun horses have different distributions of pigment-producing cells.
KITLG encodes KIT ligand, a molecule required for melanocyte migration and survival in the skin and hair follicle.
Non-dun1 has a guanine where dun has an adenine at chromosome 8 base pair 18,226,905, which appears to be sufficient to cause non-dun1 coloration.