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What are the genetics of horse coat color?

The coat color of horses is determined by a number of different genetic factors that control the production and distribution of pigments. Understanding the genetics behind horse colors and patterns can help breeders select for desired traits and avoid unwanted surprises in foal coats. In this comprehensive guide, we will explore the many genes involved in equine coat color and their various interactions and effects.

The Basics of Horse Pigmentation

There are two basic pigments that contribute to coat color in horses:

  • Eumelanin – A dark brown/black pigment
  • Pheomelanin – A red/yellow pigment

The distribution and ratio of these two pigments across the body determines the basic coat color. For example, a horse with mostly eumelanin will be some shade of black, while a higher pheomelanin concentration produces chestnut or sorrel coats.

These pigments are produced by cells called melanocytes in the skin and hair follicles. Several main genes control whether melanocytes will produce more eumelanin, pheomelanin, or no pigment at all. Additional genes then act as modifiers to alter the final coat pattern and shade.

The Extension Gene

The most important gene controlling the base production of pigment is the extension gene. This gene codes for the protein melanocortin 1 receptor (Mc1r), which binds to melanocyte stimulating hormone and stimulates eumelanin synthesis.

The dominant allele (E) results in a fully functional receptor and black pigment production. The recessive allele (e) causes a loss of function and only pheomelanin production. This creates three basic phenotypes:

  • EE or Ee – Black pigment (bay, black)
  • ee – Red pigment only (chestnut, sorrel)

The extension gene sets the stage for all the other coat color genes by controlling this first key step in pigment type.

The Agouti Gene

While the extension gene determines whether eumelanin can be produced at all, the agouti gene controls where and how much of this black pigment gets distributed across the body. This gene regulates the alternate binding of hormones that stimulate eumelanin vs. pheomelanin production in the hair follicle growth cycle.

The dominant allele (A) results in agouti signaling protein being produced, which causes a shift from eumelanin to pheomelanin production partway up each hair. This results in black pigment at the base of hairs and reddish bands further up, creating a tan coat with black points and manes/tails. Examples are bay, brown, or wild bay horses.

The recessive allele (a) causes uniform production of eumelanin throughout each hair without the banding shift. This produces a solid black coat color in horses with at least one E extension gene. Examples are black, smoky black, or seal brown horses.

The key phenotypes for agouti are:

  • A_ – Bay horse with black legs, mane and tail
  • aa – Black horse with no light areas

The Gray Gene

The gray gene is one of the most striking and dominant coat color genes. The dominant G allele causes progressive depigmentation and a transition from a horse’s original coat color to almost completely white over time. Most gray horses are born bay, black, or chestnut and undergo gradual greying starting around the face and eyes.

A single copy of G is enough to cause graying, so genotypes of GG, Gg, or G- result in gray coats. Two recessive alleles (gg) are needed to avoid the gray factor.

Graying can complete by 6-8 years old, but full whitening often takes longer. The pattern of progression and final degree of whitening can vary quite a bit between horses. Gray does not affect skin pigmentation, so many “white” gray horses still have dark skin and eyes.

The Cream Gene

The cream dilution gene produces paler coat shades by reducing the concentration of pigment in the hair. The dominant allele (CCr) inhibits movement of pigment granules from melanocytes into hair shaft melanosomes during development.

A single copy dilutes black to smoky or reddish coats to gold champagne. Two copies (CCrCCr) cause even greater dilution to cremello or perlino. The recessive genotype cc results in no dilution.

Some key cream dilutions are:

  • Black to smoky black
  • Bay to buckskin
  • Chestnut to palomino
  • Black to cremello
  • Sorrel to perlino

The Dun Gene

The dun gene is easy to spot based on its trademark primitive markings. The dominant allele (D) causes distinct leg and spine striping along with shoulder bars, leg barring, and sometimes ear tips and facial masking.

Dun only affects black pigmented areas, so it can be combined with any base coat color. Examples are bay dun, buckskin dun, grullo (black + dun), and red dun on a chestnut base.

One or two copies of D produce the dun phenotype. The recessive dd genotype shows no primitive markings.

The Roan Gene

Roan is one of the rarer coat patterns in horses. It is characterized by an even mix of white and colored hairs interspersed together. Breeds like Quarter Horses, Paints, and Appaloosas can carry roan.

This pattern is caused by the dominant Rn allele of the roan gene. Roan is expressed similarly whether heterozygous (Rn-) or homozygous (RnRn). The white hairs develop gradually as horses age.

Common roan colors are bay roan, red roan, and blue roan on a black base coat. Roan can be combined with other dilutions like palomino or buckskin.

The recessive genotype rnrn does not produce roaning. Breeding two roan horses together often results in a higher white hair concentration in offspring.

The Sabino Gene

Sabino is a white spotting pattern characterized by high white on legs, belly spots, face blazes, and jagged spotting. It occurs due to the dominant SB1 allele. Horses with SB1- or SB1SB1 have extensive white markings.

Common patterns are splashed white, Medicine Hat paints, and maximum sabino whites. Minimal expression causes modest white leg markings and face blazes.

Overo paint patterns in breeds like American Paint Horses are due to combinations of sabino with framing mutations. The recessive sb1sb1 genotype shows no sabino traits.

The Dominant White Gene

The dominant white gene (W) is the most dramatic white spotting gene. Just one copy can produce completely white or near-white coats with pink skin and brown eyes.

Dominant white arises from mutations in the KIT gene involved in melanocyte migration and survival during development. Heterozygous W- horses have variable expression ranging from all-white to minimal sabino-like spotting.

When two dominant white alleles are inherited (WW), the complete lack of melanocytes is typically lethal. The recessive genotype ww has no effect on pigmentation.

The Appaloosa Pattern Gene (LP)

The Appaloosa spotting pattern occurs almost exclusively in the Appaloosa breed. It is caused by an incompletely dominant allele, LP. Homozygous LPLP horses have the most pronounced spotting, while LPlp produces fewer spots.

Appaloosas have combinations of white sclera around the eyes, striped hooves, mottled skin, and sparse colored spotting on a white base coat. Complex interactions between LP and other genes influence the final amount and placement of pigmented spots.

Horses with the lp/lp genotype do not exhibit any Appaloosa characteristics. LP is very rare outside of the Appaloosa population.

The Tobiano Gene (TO)

Tobiano is one of two common genes producing the overo-type paint coat patterns. It is caused by an incompletely dominant allele (TO).

Tobiano results in large patches of pigment and white arranged vertically down the body. The head usually has high white, legs are often white, and spots usually cross the topline. Each copy of TO increases the amount of white and extent of spotting.

Breeds like American Paint Horses have selectively bred for tobiano patterns. The recessive genotype (toto) does not produce any spotting.

The Frame Overo Gene (O)

Frame overo spotting is the other common type of painted pattern in horses. It is caused by a dominant allele (O) of the frame overo gene.

Instead of large vertical areas of color, overos have jagged color patterns with more horizontal orientation. The white does not usually cross the topline. Extensive leg and head white are hallmarks of frame overo.

When homozygous (OO), frame overo can cause lethal white foal syndrome. Breeding two frame overos together is not recommended due to this risk. Solid coat horses have the genotype oo.

The Splashed White Gene (SW)

Splashed white causes dramatic, extensive white markings and blue eyes. It is an incomplete dominant gene (SW) with variable expression.

Typical features are largely pink facial skin, white legs with sharp horizontal borders, white belly spots, and blue eyes. More white generally occurs with increasing copies of SW.

It interacts with other paint genes like tobiano to produce uniquely patterned coats. Horses with non-splashed genotypes (swsw) do not have splash characteristics.

Summary of Major Equine Coat Color Genes

Gene Effect of Dominant Allele Example Phenotypes
Extension Allows production of black pigment Bay, black, brown
Agouti Causes banded hairs with red and black Bay, wild bay, brown
Gray Causes progressive greying with age Dapple gray, flea bitten gray
Cream Dilutes red to gold and black to smoky Buckskin, cremello, smoky black
Dun Produces primitive markings Bay dun, grullo, red dun
Roan Causes equal mix of white and colored hairs Bay roan, blue roan
Sabino Irregular spotting, high leg white Minimal sabino, max sabino
Dominant White Extensive, often all-white coat White, near-white
Appaloosa Coat spotting, striped hooves Few spot leopard, snowcap blanket
Tobiano Vertical pigment patches Tobiano paint horse
Frame Overo Irregular horizontal spotting Frame overo paint
Splashed White Dramatic white markings and blue eyes Splashed white paint

Interactions Between Genes

With so many coat color genes interacting, the genotypes can become quite complex. Some key examples of gene interactions include:

  • Agouti only affects black pigment, so aa has no effect on ee red horses
  • Cream and gray together gradually dilute to white
  • Roan can occur on any base coat color
  • Dun only affects black points, so is visible on bay but not black
  • Sabino enhances white markings produced by other paint genes
  • Dominant white epistatic to all other coat genes
  • LETHAL: Homozygous frame overo (OO) often causes death

With many possible allele combinations, breeders must understand the genetic interactions to avoid unwanted results like lethal white foals or excessive white markings.

Breed Differences in Coat Color Genes

The frequencies of various coat color genes and alleles can vary significantly between horse breeds. This gives many breeds their distinctive color characteristics:

  • Thoroughbreds – Almost exclusively bay, chestnut, black due to selective breeding. No cream or dun.
  • Arabians – High frequency of gray gene. Also sabino roaning common.
  • Appaloosas – LP gene mutations cause characteristic coat spotting.
  • Quarter Horses – Tobiano, frame overo, splash white produce common paint patterns.
  • Miniatures – Roan and tobiano genes predominate.
  • Morgans – Sabino influence gives high white facial and leg markings.
  • Icelandic Horses – Unique genetic variant causes the “Icelandic” coat pattern.

But rare variants can still occur in any breed. Genetic testing allows breeders to screen their stock for desired or undesired alleles.


Equine coat color is a complex but fascinating product of genetic interactions. From the basic bay, black, and chestnut horses to exotic pinto patterns and dilutions, it’s remarkable to see the diversity that can be achieved from combinations of a handful of key genes. An understanding of the underlying genetics allows breeders to make informed selections when trying to achieve their ideal coat colors and patterns.