HOME       LINKS      MAIL








Coat Color

Coat Colors

Color Requirements

Perlino Paints (pdf) - Positively Perlino by Rebecca Overton

Paint Horse Journal February 2001• Volume 35, Number 2

Roan Genetics (pdf) - The White Stuff by Rebecca Overton - Paint Horse Journal January 2002 • Volume 36, Number 1

Gray isn't a color (pdf) - Tarcy Ganz - Paint Horse Journal August 2006 • Volume 40, Number 8

Dun Zygosity Test - UC Davis Veterinary Genetics Laboratory, CA

Coat Color Test - UC Davis Veterinary Genetics Laboratory, CA

Offspring Coat Color Calculator - Animal Genetics Incorporated


Blue Eyes

The colors that have blue eyes are Double Dilutes, Splashed Whites, Frame Overos, and some Champagnes. Tobianos, Sabinos, Duns and solids do not have blue eyes unless the horse also has one of these patterns or dilutions. 

Coat Color Genetics and Blue Eyes - Morgan Hutchings, Danger Ranch, Addison, AL


A true homozygous Paint horse is always a tobiano. The homozygous horse has two identical tobiano genes and must be sired by a tobiano, and have a tobiano for a mother. The true homozygous tobiano must have secondary body spotting called "ink spots" and "paw prints" and must never have produced any solid colored foals from solid colored mates.

Homozygous Tobianos will always pass a tobiano gene to an offspring (genes TT). The majority of homozygous tobiano stallions standing today, sire 100% tobiano paint colored foals from the mares they breed. A few horses that are listed as homozygous, have sired the occasional solid breeding stock foal, but this is rare.

Ink Spots and Paw Print Markings are unique and distinctive markings and usually located in the 'white' hair areas on a tobiano and are small dabs of spots or color (1-3 inches) surrounded with prominent "blue zones" (white hairs on black pigmented skin that give the hair a blue appearance) surrounding the 'spot'. Usually there will be groups of prints that look like dog or cat tracks. The black homozygous tobiano shown above has nice examples of these markings and there is a larger photo on the "Overo-Tobiano-Tovero" web page. These patterns tend to show up on homozygous individuals, who have two tobiano genes, but also occur on heterozygous tobiano horses who only have one tobiano gene.

In a horse classified as "informative", the hair marker of the individual can be used as indicator to test their offspring for homozygous tobiano status. In an "uninformative" horse, the hair marker of this individual do not confirm the tobiano status of their foals, so the ability of this horse to consistently sire or produce colored foals, cannot be determined.

Horse Tests - Tobiano - UC Davis Veterany Genetics laboroatory, CA

Black Pigment Gene

A red coat color in horses is well-documented to be inherited as a trait recessive to black. A diagnotic test for the red factor, based on DNA analysis, provides the information to determine what color offspring a horse can throw. The absence of the red factor presents itself as "E".

"E" - No red factor was detected. The horse can be assumed to be homozygous for black pigment (EE). It cannot have red foals (sorrel or chestnut) regardless of the color of the mate. The basic color of the horse will be black, bay or brown, but may also have buckskin, zebra dun, grulla, perlino, gray, white or any of these colors with the white hair patterns of tobiano for Paints.  

Coat Color Test - UC Davis Veterinary Genetics Laboratory, CA

Barlink Factor

In the study of what "is" champagne, one also needs to address what "is not" champagne. Several horses have been presented to me over the past several months as "possible champagnes" who are not. All of these horses are related to the Paint stallion, Barlink Macho Man, a chestnut splashed white/frame overo. The Barlink factor dilution gene is not champagne, but can mimic it. I believe this gene has not yet been described in the literature. It appears to work as an incomplete dominant, similar to the cream gene, and also enhances the cream gene, as does champagne.

In single dose, the Barlink factor appears to dilute the skin of the carriers. The chestnuts with submitted photographs have pink speckles on their otherwise black skin, very similar to what happens on many cream dilutes. The gene is not cream, as these mares do not demonstrate the cream gene when tested by UC Davis. With a single Barlink gene, the coat color does not seem to be affected.

In double dose, the Barlink factor appears to dilute the hair coat to a medium dilute shade (similar to one cream or one champagne gene), and dilutes the skin to near pink.

The Barlink factor appears to enhance cream, essentially causing a double dilution of the hair coat, skin and eyes. This would cause the phenomenon of pseudo-cremello and pseudo-smoky cream foals. I have not yet seen the effect on buckskin, but it is likely a pseudo-perlino would result.

While this proposed new Barlink dilution gene can resemble champagne, it is not. Thus, future Barlink related horses submitted for registration with the ICHR will be scrutinized more closely, and will need to demonstrate champagne in the immediate pedigree before being accepted into the registry.

The Barlink Factor (pdf) - Champagne Horse Journal, Carolyn Shepard, July 2002

Champagne Delusion (pdf) - The Barlink Paints, the Lusitano dilutes and the "Spud" factor - Champagne Horse Journal, Carolyn Shepard, Fall 2003



Overo Lethal White Syndrome (OLWS) is a condition that occurs in newborn foals. The condition is genetic, and both parents carry the defective gene. Horses that carry this gene are most commonly overo white patterned horses (frame overos), but there are exceptions. The defective gene has been found in American Paint Horses, American Miniature Horses, Half-Arabians, Thoroughbreds, and cropout Quarter Horses (foals born to registered Quarter Horse parents that have too much white to qualify for registration with the American Quarter Horse Association).

OLWS foals have blue eyes and are completely or almost completely white at birth. These foals initially appear normal except for their unusual coloring. After a varying period of time, troubling signs of colic emerge due to the foal's inability to pass feces. The OLWS foal has an underdeveloped, contracted intestine caused by a failure of the embryonic cells that form nerves in the gastrointestinal system. Oddly enough, these cells also play a role in determining skin color.

There is no treatment for OLWS, and surgery to bypass the intestinal damage has never been successful due to the extensive nature of this type of lesion. Veterinarians advise euthanasia for all OLWS foals because death will inevitably occur from colic caused by fatal constipation.

Lethal Whites: A Light at the End of the Tunnel
Several experts clarify what we now know, and what we hope to know soon about this devastating syndrome. By Dawn Walker, from the February 1997 Paint Horse Journal

Stalking the Lethal White Syndrome
University of Minnesota researchers track down the gene responsible for lethal white foals. By Paul D. Vrotsos RVT and Elizabeth M. Santschi DVM, from the July 1998 Paint Horse Journal

UC-Davis Horse Genetics

Testing for Lethal White (pdf) - By A Hair by Rebecca Overton - Paint Horse Journal, March 2004 • Volume 38, Number 3


Hyperkalemic Periodic Paralysis, commonly known as HyPP, has been widely spread throughout the equine industry over the last several years. This heritable disease is caused by a genetic defect that has been found through research to trace back to the great Quarter Horse stallion, Impressive.

HyPP affects the sodium channels of afflicted horses and overloads the system with high potassium levels that cause episodes which may include: mild muscle twitching that is undetectable to the human eye; noticeable muscle twitching; "crawling" skin, ranging from slight to very noticeable and usually from the back flank area forward; hind quarter paralysis; excessive yawning; and paralysis of the muscles surrounding the heart and/or lungs, causing death due to heart attack or suffocation. Not all horses affected with HyPP will show outward signs and will live full productive lives.

HyPP was identified in 1985, and a test was made available for public use in 1992. When the test was made available to the public, breeders were encouraged to test their breeding stock and choose horses who did not carry HyPP to be used as breeding stock.

January 1, 2007 was the date set to no longer allow registry of foals testing H/H at the 2004 AQHA convention. Mandatory testing for HyPP was also put into ruling at the convention. N/H was not ruled against at that time.

The Appaloosa Association followed suit with their date to disallow registry of HH foals beginning January 1, 2008.

The APHA did not pass rulings in any category at their 2004 convention.

There are three testing statuses for HyPP:

  • H/H - This status means that a horse carries a double copy of the defective gene and will pass at least one copy of the gene and the disease to 100% of it's offspring.

  • N/H - This status means that the horse carries one normal gene and one HyPP gene and will pass the gene and the disease, on average, to 50% of it's offspring. some N/H horses will pass it to more and some to less than the average, but collectively, it will pass on to 50%. N/H to N/H cross will beget 25% N/N, 50% N/H, and 25% H/H

  • N/N - This status means that the horse carries two normal genes. It does not have the disease, nor can it be passed on.

HyPP Factts- UCDavis, Current Facts About Hyperkalemic Periodic Paralysis (HYPP) Disease


Hereditary equine regional dermal asthenia (HERDA) is a genetic skin disease predominantly found in the American Quarter Horse. Within the breed, the disease is prevalent in particular lines of cutting horses. HERDA is characterized by hyperextensible skin, scarring, and severe lesions along the back of affected horses. Affected foals rarely show symptoms at birth. The condition typically occurs by the age of two, most notably when the horse is first being broke to saddle. There is no cure and the majority of diagnosed horses are euthanized because they are unable to be ridden and inappropriate for future breeding. HERDA has an autosomal recessive mode of inheritance and affects stallions and mares in equal proportions. Research carried out in Dr. Danika Bannasch's laboratory at the University of California, Davis has identified the gene and mutation associated with HERDA.

The diagnostic DNA test for HERDA that has been developed allows identification of horses that are affected or that carry the specific mutation. Other skin conditions can mimic the symptoms of HERDA. The DNA test will assist veterinarians to make the correct diagnosis. For horse breeders, identification of carriers is critical for the selection of mating pairs. Breedings of carrier horses have a 25% chance of producing an affected foal. Breedings between normal and carrier horses will not produce a HERDA foal although 50% of the foals are expected to be carriers.

< xml="true" ns="urn:schemas-microsoft-com:office:office" prefix="o" namespace="">

Horse Tests - UC Davis Veterinary genetics Laboratory, CA

Wobbler's Syndrome

Wobbler disease is a condition of the cervical vertebrae that causes an unsteady (wobbly) gait and weakness in dogs and horses. The term wobbler disease refers to a number of different conditions of the cervical (neck) spinal column that all cause similar symptoms. These conditions may include malformation of the vertebrae, intervertebral disc protrusion, and disease of the interspinal ligaments, ligamenta flava, and articular facets of the vertebrae.[1] Wobbler disease is also known as cervical vertebral instability, cervical spondylomyelopathy (CSM), and cervical vertebral malformation (CVM). In dogs, the disease is most common in large breeds, especially Great Danes and Dobermanns. In horses, it is not linked to a particular breed, though it is most often seen in tall race-bred horses. It is most likely inherited in dogs, it may be hereditary to some extent in horses.

Wobbler disease is found in dogs and horses, where it is often called Wobbler's Syndrome, refers to several conditions beyond those listed above, including equine wobbles anemia. It is also used as a catchall phrase within the horse community to designate a neurological problem that has no more specific diagnosis. Some forms, such as cervical vertebral malformation (CVM), are not thought to be hereditary, but rather a congenital condition or a growth disorder. Other forms, such as Equine wobbles anemia, are concentrated in certain breeds and may be hereditary to some extent. Horses with wobbler disease often exhibit ataxia, show weakness in the hindquarters, or may knuckle over in their fetlocks, particularly in the rear. With advanced stages of the disease they are prone to falling. While some cases are successfully treated with nutritional and medical management, surgery is also used. One method is the use of Titanium baskets, placed to fuse the vertebrae, thereby preventing compression of the spinal cord. Some horses are able to return to work, with a few able to reaching competitive levels. There is currently no complete "cure" for the condition.

Because wobbler's is the best known of the neurological conditions that affect horses, other, unrelated conditions, such as Equine Protozoal Myeloencephalitis and cerebellar abiotrophy are sometimes misdiagnosed as wobbler's, even though the causes and symptoms differ.

Commonly affected horse breeds:
American Quarter Horse
American Paint Horse

From Wikipedia, the free encyclopedia


Back to Top