dun" or a "dunskin". On such horses, the light-shaded primitive markings are most noticeable during the summer months, when the winter hair sheds. A palomino that also carries dun, showing primitive dorsal striping or leg bars indicative of a red dun may be called a "dunalino." Countershading of nd1may be harder to differentiate between a dorsal stripe on light-colored horses such as red duns. Genetics There are three known alleles of the dun gene: dun (D), non-dun1 (d1), and non-dun2 (d2). Dun is dominant, so the phenotype of a horse with either one or two copies of the gene is dun. In effect, two non-dun parents cannot produce a dun foal. Horses that are non-dun1 d1/d1 or d1/d2 may have some asymmetry in pigment distribution, producing primitive markings, but to a lesser degree than dun horses. Homozygous non-dun1/non-dun1 horses typically have clearer primitive markings than heterozygous d1/d2 horses. The primitive markings from non-dun1 are more visible on a bay or chestnut horse; they blend in on a black. A horse with two copies of non-dun2 lacks primitive markings. Dun has a stronger effect than other dilution genes in that it acts on any coat color. In contrast, the silver dapple gene acts only on black-based coats, and the cream gene is an incomplete dominant which must be homozygous to be fully expressed, and when heterozygous is only visible on bay and chestnut coats, and then to a lesser degree. The dun dilution effect is caused by pigment only being placed in a part of each hair. Specifically, hairs from diluted areas only have pigment along one side of them, while hairs from darker parts such as the dorsal stripe have pigment all the way around. Genetic analysis and DNA sequencing results published in 2015 link dun color to the T-box 3 (TBX3) transcription factor. When functional, it creates dun coloring, including the primitive markings, and when recessive, a horse is not dun. In humans and lab mice, TBX3 is critical to development. 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. In non-dun horses, the TBX3 protein is still functional, and is still produced in most cells, but not expressed in the hair cortex. Where the coat is diluted, the color is not uniform throughout each hair, but rather