Ann T. Bowling

Last updated

Ann T. Bowling
Ann Bowling.gif
Born
Ann Trommershausen

(1943-06-01)June 1, 1943
Portland, Oregon, US
DiedDecember 8, 2000(2000-12-08) (aged 57)
Davis, California, US
NationalityAmerican
Alma mater
Known forThe Genetics of the Horse (2000); Horse Genetics (1997)
SpouseMichael Bowling
Children1
Scientific career
Fields Genetics
Institutions University of California, Davis
Thesis A morphological, histological, and biochemical study of the tomato mutant 'curl'  (1969)
Doctoral advisor G. Ledyard Stebbins

Ann Trommershausen Bowling (June 1, 1943 – December 8, 2000) was an American scientist who was one of the world's leading geneticists in the study of horses, conducting research in the areas of molecular genetics and cytogenetics. [1] She was a major figure in the development of testing to determine animal parentage, first with blood typing in the 1980s and then DNA testing in the 1990s. She later became known for her studies of hereditary diseases in horses and equine coat color genetics, as well as research on horse evolution and the development of horse breeds. She studied the population genetics of feral horses, did considerable work to help preserve the Przewalski's horse, and was one of the founding members of the international project to map the horse genome. [1] [2] [3] She was an adjunct professor at the University of California, Davis (UCD), and at the time of her death in 2000 was the executive associate director of the Veterinary Genetics Laboratory (VGL) there. Her unexpected death on December 8, 2000, at age 57 was attributed to a massive stroke. [1]

Contents

Early life and career

Ann Bowling (née Trommershausen) was born June 1, 1943, in Portland, Oregon, to Claire Bowen and William Ernest Trommershausen, [4] who worked for the Bonneville Power Administration. [5] After the Trommershausens moved to Boulder, Colorado, Ann attended Boulder High School and was class valedictorian. She obtained her undergraduate degree at Carleton College in Minnesota, graduating magna cum laude . [4]

She earned her PhD in 1969 at the University of California, Davis, completing her thesis on the genetics of plants under the supervision of G. Ledyard Stebbins. [4] [6] She joined the faculty of Occidental College in Los Angeles in 1968, then was hired by UC Davis in 1973, [4] and at the time of her death in 2000 was an adjunct professor and executive associate director of the Veterinary Genetics Laboratory (VGL) at UC Davis. [1] [3]

She married Michael Bowling in 1981. [4] Both members of the couple shared a strong interest in genetics; prior to their marriage, Ann used Michael's stud book research in her own 1980 study of genetic diseases. [7] Michael Bowling wrote a number of articles on Arabian horse genetics for general-interest publications, [lower-alpha 1] and the pair collaborated on a study of mtDNA in Arabian bloodlines. [11] Their daughter Lydia attended veterinary school and UC Davis and became a veterinarian. [12] [13] [14]

Animal parentage identification

Bowling developed some of the first blood typing and DNA parentage tests for horses, and became a genetics consultant to several horse breed registries, including The Jockey Club, Arabian Horse Association (originally Arabian Horse Registry of America), American Quarter Horse Association, and the American Morgan Horse Association. [2] Beginning in 1976, she published research on animal blood types, [15] [16] [17] and developed tests using blood type to establish parentage. [18] She advocated for adopting blood typing for parentage verification of registered animals. Numerous breed registries did so. [2] In the course of this research, she also studied the phenomenon of chimerism, which sometimes created inconsistent results in parentage testing. [19]

By the late 1990s, as the science of parentage testing evolved, she researched the effectiveness of DNA typing and concluded that it was as effective as blood typing for verifying parentage. [20] Her lab pioneered the DNA-based parentage verification of horses and camelids —species for which Bowling herself had conducted research [lower-alpha 2] —using microsatellites as biomarkers. [21] This testing program also expanded to include eight other types of mammals. [21]

Bowling applied her work on identifying parentage to help preserve the genetic diversity of the Przewalski's horse. Among other work, she reconstructed the herd book of the captive Askania Nova herd in Ukraine using parentage testing data. [2] She studied the genetics of Mustangs in the Great Basin and located genetic markers linking them to other domesticated horse breeds. [22] She also performed research on the blood types of the Paso Fino breed. [23]

Some of the more unusual work the VGL performed was a 1996 investigation by Scotland Yard, which sought help from the lab to identify the source of a blood sample associated with a murder. The lab identified the sample as being from a dog that was at the crime scene, and this information helped crack the case by leading investigators to a suspect who was the owner of the dog. Bowling was the director of the laboratory at the time, and as a result of this work, expanded the lab's scope so it could continue to help identify animals present at crime scenes and those animals which themselves were victims of crimes such as theft or animal abuse. From this beginning, the VGL also later helped create a national canine database used to prosecute cases of dogfighting. [21] Bowling also published articles on parentage in mules, including a case where she proved the rare occurrence of a fertile mule mare by parentage testing. [lower-alpha 3]

Genetic disease and equine coat color research

From very early in her career, Bowling wrote about educating horse breeders on genetic diseases in purebred animals and how to deal with these conditions. [24] She performed a number of studies on the Arabian horse breed, including research into one of the genetic diseases that affects Arabians, cerebellar abiotrophy (CA). In 1985, she created a breeding herd at UCD of horses known to carry CA, and this small group provided preliminary DNA data for researchers. [25] Bowling's own studies of CA were unpublished at the time of her death, but she is credited with demonstrating that the condition had a recessive mode of genetic inheritance and was likely the result of a single mutated allele. [26] A DNA marker test for the condition was developed by her successors at UCD, which became available to the public in 2008. [27] In 2011, the causative mutation for cerebellar abiotrophy was identified, and the condition was conclusively established as an autosomal recessive. [28]

Bowling also studied genetic conditions in other horse breeds, including hyperkalemic periodic paralysis (HYPP) in the American Quarter Horse. In 1996, her research found that the origin of this genetically dominant disorder traced to a single stallion, [29] later identified publicly as Impressive. [30]

Bowling's study of equine coat color genetics originally coincided with her studies of animal parentage. [15] [lower-alpha 4] Research related to equine coat colors dovetailed with genetic disease research when she studied overo spotting patterns seen in Paint horses. [31] She was part of a research team that studied lethal white syndrome (LWS), a fatal condition in newborn foals. [32] [33] She had authored an early study in 1977 that ruled out neonatal isoerythrolysis as a cause of death. [34] In 1983, the team linked LWS to a coat color spotting pattern, [32] later identified as frame overo, which is seen in the American Paint Horse and related breeds. [35] In 1997 Bowling was one of three researchers to identify the gene responsible for LWS, and in the process identified the condition as the equine version of Hirschsprung disease. [36] [37]

While researching lethal white syndrome, Bowling also studied the phenomenon of cropouts; spotted offspring born from two minimally-marked parents. [31] She also worked with the team that mapped the cream gene, [38] which is a dilution gene with no deleterious effects, though a misconception exists that cream colors might be linked to lethal white syndrome. [39] [40]

In addition to her work on deleterious mutations associated with horse genetics, Bowling studied genetic disorders in the Australian shepherd dog that appeared to be linked to the merle coat color. [41]

Horse genome project

In the 1990s, Bowling was one of the leaders in the horse genome project. [42] This work was also important to human medicine, as there are at least 90 genetic conditions that can affect both humans and horses. [43] The horse genome was first sequenced in 2006, [44] and was fully mapped by 2009. [45]

Horse breeding

Bowling owned Arabian horses, and was a co-founder of the New Albion Stud along with her husband Michael and her parents, Bill and Claire Trommershausen. [2] Ann and her parents had owned half-Arabians when they lived in Colorado; Michael Bowling had owned Arabians since 1962. They started the farm in September 1980, about the same time that Ann and Michael married, and placed an emphasis on bloodlines descended from the Crabbet Arabian Stud. The farm continued to be operated by her husband and daughter after Bowling's death. [14] Bowling's study of mitochondrial DNA in Arabians found that pedigree records kept by the American registry for Arabian horses were generally reliable from the time of importation forward. But her work also brought into question a belief commonly held by Arabian breeders that horses imported from the desert identified by specific historic dam lines or "strains" in their pedigrees actually traced to specific matrilineal groups. Bowling also found that some mare lines claimed to originate from the same desert-bred "strain" were not related at all, and some mares whose pedigrees claimed they were of different strains turned out to be distantly related. [11]

Publications

Bowling was the author or coauthor of two books and 93 scientific journal articles, [4] including:

Books

Journals

Notes

  1. ↑ Michael Bowling's work has included, but is not limited to study of SCID, [8] preservation breeding, [9] genetic diseases in horses generally, and Crabbet Arabian bloodlines. [10]
  2. ↑ see, e.g. Juneja, RK; Penedo, MC; Larsson, HE; Gahne, B; Bowling, AT (1989). "Two-dimensional electrophoresis of the plasma proteins of alpacas and llamas: genetic polymorphism of alpha 1B-glycoprotein and three other proteins". Animal Genetics. 20 (4): 395–406. doi:10.1111/j.1365-2052.1989.tb00895.x. PMID   2619106.; Penedo, MC; Fowler, ME; Bowling, AT; Anderson, DL; Gordon, L (1988). "Genetic variation in the blood of llamas, Llama glama, and alpacas, Llama pacos". Animal Genetics. 19 (3): 267–76. doi:10.1111/j.1365-2052.1988.tb00815.x. PMID   3207220.
  3. ↑ see, e.g. Ryder, OA; Chemnick, LG; Bowling, AT; Benirschke, K (September–October 1985). "Male mule foal qualifies as the offspring of a female mule and jack donkey". The Journal of Heredity. 76 (5): 379–81. PMID   4056372.; Bowling, AT; Nickel, LS (January–February 1985). "Inheritance of Equus asinus serum albumin variants in hybrid offspring". The Journal of Heredity. 76 (1): 73–4. doi:10.1093/oxfordjournals.jhered.a110028. PMID   3980976.
  4. ↑ Bowling originally sought to verify if foals recorded as having genetically impossible coat colors given their parentage were due to recordkeeping errors by breed registries. [15]

Related Research Articles

<span class="mw-page-title-main">Standardbred</span> American breed of horse

The Standardbred is an American horse breed best known for its ability in harness racing, where members of the breed compete at either a trot or pace. Developed in North America, the Standardbred is recognized worldwide, and the breed can trace its bloodlines to 18th-century England. They are solid, well-built horses with good dispositions. In addition to harness racing, the Standardbred is used for a variety of equestrian activities, including horse shows and pleasure riding, particularly in the Midwestern and Eastern United States and in Southern Ontario.

<span class="mw-page-title-main">Palomino</span> Genetic color in horses

Palomino is a genetic color in horses, consisting of a gold coat and white mane and tail; the degree of whiteness can vary from bright white to yellow. Genetically, the palomino color is created by a single allele of a dilution gene called the cream gene working on a "red" (chestnut) base coat. Palomino is created by a genetic mechanism of incomplete dominance, hence it is not considered true-breeding. However, most color breed registries that record palomino horses were founded before equine coat color genetics were understood as well as they are today, therefore the standard definition of a palomino is based on the visible coat color, not heritability nor the underlying presence of the dilution gene.

<span class="mw-page-title-main">Lethal white syndrome</span> Medical condition

Lethal white syndrome (LWS), also called overo lethal white syndrome (OLWS), lethal white overo (LWO), and overo lethal white foal syndrome (OLWFS), is an autosomal genetic disorder most prevalent in the American Paint Horse. Affected foals are born after the full 11-month gestation and externally appear normal, though they have all-white or nearly all-white coats and blue eyes. However, internally, these foals have a nonfunctioning colon. Within a few hours, signs of colic appear; affected foals die within a few days. Because the death is often painful, such foals are often humanely euthanized once identified. The disease is particularly devastating because foals are born seemingly healthy after being carried to full term.

<span class="mw-page-title-main">Gray horse</span> Coat color characterized by progressive depigmentation of the colored hairs of the coat

A gray horse has a coat color characterized by progressive depigmentation of the colored hairs of the coat. Most gray horses have black skin and dark eyes; unlike some equine dilution genes and some other genes that lead to depigmentation, gray does not affect skin or eye color. Gray horses may be born any base color, depending on other color genes present. White hairs begin to appear at or shortly after birth and become progressively more prevalent as the horse ages as white hairs become intermingled with hairs of other colors. Graying can occur at different rates—very quickly on one horse and very slowly on another. As adults, most gray horses eventually become completely white, though some retain intermixed light and dark hairs.

<span class="mw-page-title-main">Silver dapple gene</span>

The silver or silver dapple (Z) gene is a dilution gene that affects the black base coat color and is associated with Multiple Congenital Ocular Abnormalities. It will typically dilute a black mane and tail to a silvery gray or flaxen color, and a black body to a chocolaty brown, sometimes with dapples. It is responsible for a group of coat colors in horses called "silver dapple" in the west, or "taffy" in Australia. The most common colors in this category are black silver and bay silver, referring to the respective underlying coat color.

<span class="mw-page-title-main">Equine coat color genetics</span> Genetics behind the equine coat color

Equine coat color genetics determine a horse's coat color. Many colors are possible, but all variations are produced by changes in only a few genes.

Glycogen-branching enzyme deficiency (GBED) is an inheritable glycogen storage disease affecting American Quarter Horses and American Paint Horses. It leads to abortion, stillbirths, or early death of affected animals. The human form of the disease is known as glycogen storage disease type IV.

<span class="mw-page-title-main">Overo</span> Group of colouration patters of horses

Overo refers to several genetically unrelated pinto coloration patterns of white-over-dark body markings in horses, and is a term used by the American Paint Horse Association to classify a set of pinto patterns that are not tobiano. Overo is a Spanish word, originally meaning "like an egg". The most common usage refers to frame overo, but splashed white and sabino are also considered "overo". A horse with both tobiano and overo patterns is called tovero.

<span class="mw-page-title-main">Chestnut (horse color)</span> Horse coat color

Chestnut is a hair coat color of horses consisting of a reddish-to-brown coat with a mane and tail the same or lighter in color than the coat. Chestnut is characterized by the absolute absence of true black hairs. It is one of the most common horse coat colors, seen in almost every breed of horse.

<span class="mw-page-title-main">Equine coat color</span> Horse coat colors and markings

Horses exhibit a diverse array of coat colors and distinctive markings. A specialized vocabulary has evolved to describe them.

<span class="mw-page-title-main">Cerebellar abiotrophy</span> Genetic condition in animals

Cerebellar abiotrophy (CA), also called cerebellar cortical abiotrophy (CCA), is a genetic neurological disease in animals, best known to affect certain breeds of horses, dogs and cats. It can also develop in humans. It develops when the neurons known as Purkinje cells, located in the cerebellum of the brain, begin to die off. These cells affect balance and coordination. They have a critical role to play in the brain. The Purkinje layer allows communication between the granular and molecular cortical layers in the cerebellum. Put simply, without Purkinje cells, an animal loses its sense of space and distance, making balance and coordination difficult. People with damage to the cerebellum can experience symptoms like unsteady gait, poor muscle control, and trouble speaking or swallowing.

<span class="mw-page-title-main">Sabino horse</span> Color pattern in horses

Sabino describes a distinct pattern of white spotting in horses. In general, Sabino patterning is visually recognized by roaning or irregular edges of white markings, belly spots, white extending past the eyes or onto the chin, white above the knees or hocks, and "splash" or "lacy" marks anywhere on the body. Some sabinos have patches of roan patterning on part of the body, especially the barrel and flanks. Some sabinos may have a dark leg or two, but many have four white legs. Sabino patterns may range from slightly bold face or leg white markings—as little as white on the chin or lower lip—to horses that are fully white.

Equine polysaccharide storage myopathy is a hereditary glycogen storage disease of horses that causes exertional rhabdomyolysis. It is currently known to affect the following breeds American Quarter Horses, American Paint Horses, Warmbloods, Cobs, Dales Ponies, Thoroughbreds, Arabians, New Forest ponies, and a large number of Heavy horse breeds. While incurable, PSSM can be managed with appropriate diet and exercise. There are currently 2 subtypes, known as Type 1 PSSM and Type 2 PSSM.

Hereditary equine regional dermal asthenia (HERDA), also known as hyperelastosis cutis (HC), is an inherited autosomal recessive connective tissue disorder. It develops from a homozygous recessive mutation that weakens collagen fibers that allow the skin of the animal to stay connected to the rest of the animal. Affected horses have extremely fragile skin that tears easily and exhibits impaired healing. In horses with HC, the skin separates between the deep and superficial dermis. There is no cure. Most affected individuals receive an injury they cannot heal, and are euthanized. Managed breeding strategy is currently the only option for reducing the incidence of the disease.

<span class="mw-page-title-main">Smoky black</span>

Smoky black or just smoky is a hair coat color of horses which appears dark brown to black in color. Smoky black is produced by the action of a heterozygous cream gene on an underlying black coat color. Therefore, smoky black is a member of the cream family of coat color dilutions, and found in horse populations that have other cream-based colors such as palomino, buckskin, perlino, cremello and smoky cream. All smoky blacks must have at least one parent with the cream gene, and a smoky black can only be verified through DNA testing or parentage. Smoky black has been mistaken for faded black, dark bay or brown, grullo or even liver chestnut.

<span class="mw-page-title-main">Lavender foal syndrome</span> Genetic disease in horses

Lavender foal syndrome (LFS), also called coat color dilution lethal (CCDL), is an autosomal recessive genetic disease that affects newborn foals of certain Arabian horse bloodlines. Affected LFS foals have severe neurological abnormalities, cannot stand, and require euthanasia shortly after birth. The popular name originates due to a diluted color of the foal's coat, that in some cases appears to have a purple or lavender hue. However, not all foals possess the lavender coat colour, and colouring can range from silver to light chestnut to a pale pink. Carrier horses have no clinical signs and DNA testing can determine if a horse carries the gene.

<span class="mw-page-title-main">Thoroughbred</span> Horse breed developed for racing

The Thoroughbred is a horse breed developed for horse racing. Although the word thoroughbred is sometimes used to refer to any breed of purebred horse, it technically refers only to the Thoroughbred breed. Thoroughbreds are considered "hot-blooded" horses that are known for their agility, speed, and spirit.

<span class="mw-page-title-main">Dominant white</span> Horse coat color and its genetics

Dominant white (W) is a group of genetically related coat color alleles on the KIT gene of the horse, best known for producing an all-white coat, but also able to produce various forms of white spotting, as well as bold white markings. Prior to the discovery of the W allelic series, many of these patterns were described by the term sabino, which is still used by some breed registries.

<span class="mw-page-title-main">Roan (horse)</span> Horse coat color pattern characterized by an even mixture of colored and white hairs on the body

Roan is a horse coat color pattern characterized by an even mixture of colored and white hairs on the body, while the head and "points"—lower legs, mane, and tail—are mostly solid-colored. Horses with roan coats have white hairs evenly intermingled throughout any other color. The head, legs, mane, and tail have fewer scattered white hairs or none at all. The roan pattern is dominantly inherited, and is found in many horse breeds. While the specific mutation responsible for roan has not been exactly identified, a DNA test can determine zygosity for roan in several breeds. True roan is always present at birth, though it may be hard to see until after the foal coat sheds out. The coat may lighten or darken from winter to summer, but unlike the gray coat color, which also begins with intermixed white and colored hairs, roans do not become progressively lighter in color as they age. The silvering effect of mixed white and colored hairs can create coats that look bluish or pinkish.

<span class="mw-page-title-main">Horse genome</span>

The horse genome was first sequenced in 2006. The Horse Genome Project mapped 2.7 billion DNA base pairs, and released the full map in 2009. The horse genome is larger than the dog genome, but smaller than the human genome or the bovine genome. It encompasses 31 pairs of autosomes and one sex chromosome pair.

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  2. 1 2 3 4 5 "Ann Bowling Memorial". California-Nevada Arabian Sport Horse Association. Archived from the original on March 12, 2016. Retrieved March 10, 2016.
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  16. ↑ Bowling, AT (February 1985). "Assignment of foal paternity when a mare is bred to two stallions". Theriogenology. 23 (2): 347–50. doi:10.1016/0093-691x(85)90036-6. PMID   16726003.
  17. ↑ Bowling, AT; Scott, AM; Flint, J; Clegg, JB (1988). "Novel alpha haemoglobin haplotypes in horses". Animal Genetics. 19 (2): 87–101. doi:10.1111/j.1365-2052.1988.tb00795.x. PMID   3415045.
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  20. ↑ Bowling, AT; Eggleston-Stott, ML; Byrns, G; Clark, RS; Dileanis, S; Wictum, E (August 1997). "Validation of microsatellite markers for routine horse parentage testing". Animal Genetics. 28 (4): 247–52. doi:10.1111/j.1365-2052.1997.00123.x. PMID   9345720.
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  22. ↑ Bowling, AT (June 1994). "Population genetics of Great Basin feral horses". Animal Genetics. 25 (Suppl 1): 67–74. doi:10.1111/j.1365-2052.1994.tb00405.x. PMID   7943986.
  23. ↑ Bowling, AT; Nickel, LS (1992). "New A system allele of red cell alloantigens in Paso Fino horses". Animal Genetics. 23 (6): 557–9. doi:10.1111/j.1365-2052.1992.tb00179.x. PMID   1492709.
  24. ↑ Bowling, AT (November 1980). "Counselling for genetic diseases of horses". The Veterinary Clinics of North America. Large Animal Practice. 2 (2): 377–89. doi:10.1016/S0196-9846(17)30169-6. PMID   7195098.
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  27. ↑ Minnich, Beth (2011). "Cerebellar Abiotrophy Research Project at the UC Davis Veterinary Genetics Laboratory (VGL)" (PDF). Arabian Horse Foundation. Archived from the original (PDF) on June 2, 2014. Retrieved March 13, 2016.
  28. ↑ Brault, Leah S.; Cooper, Caitlin A.; Famula, Thomas R.; Murray, James D.; Penedo, M. Cecilia T. (February 2011). "Mapping of equine cerebellar abiotrophy to ECA2 and identification of a potential causative mutation affecting expression of MUTYH". Genomics. 97 (2): 121–129. doi: 10.1016/j.ygeno.2010.11.006 . PMID   21126570.
  29. ↑ Bowling, AT; Byrns, G; Spier, S (August 1996). "Evidence for a single pedigree source of the hyperkalemic periodic paralysis susceptibility gene in quarter horses". Animal Genetics. 27 (4): 279–81. doi:10.1111/j.1365-2052.1996.tb00490.x. PMID   8856926.
  30. ↑ "Hyperkalemic Periodic Paralysis (HYPP)". Veterinary Genetics Laboratory. University of California, Davis. Retrieved March 13, 2016.
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  32. 1 2 Vonderfecht, SL; Bowling AT; Cohen M (January 1983). "Congenital intestinal megacolon in white foals". Veterinary Pathology. 20 (1): 65–70. doi:10.1177/030098588302000107. PMID   6849219. S2CID   29041847.
  33. ↑ Blendinger, C; Müller, G; Bostedt, H (June 1994). "The "lethal white foal" syndrome". Tierarztliche Praxis. 22 (3): 252–255. PMID   8048034.
  34. ↑ Trommershausen-Smith, Ann (November 1977). "Lethal white foals in matings of overo spotted horses". Theriogenology. 8 (5): 303–311. doi:10.1016/0093-691X(77)90237-0.
  35. ↑ Vrotsos, Paul D.; Santschi, Elizabeth M. (July 1998). "Stalking the Lethal White Syndrome: University of Minnesota researchers track down the gene responsible for lethal white foals". Paint Horse Journal. American Paint Horse Association. Archived from the original on March 15, 2015. Retrieved May 18, 2016.
  36. ↑ Metallinos, DL; Bowling, AT; Rine, J (June 1998). "A missense mutation in the endothelin-B receptor gene is associated with Lethal White Foal Syndrome: an equine version of Hirschsprung disease". Mammalian Genome. 9 (6): 426–31. doi:10.1007/s003359900790. PMID   9585428. S2CID   19536624.
  37. ↑ Overton, Rebecca (March 1, 2004). "By A Hair" (PDF). Paint Horse Journal. American Paint Horse Association. Archived from the original (PDF) on March 8, 2008. Retrieved September 6, 2008.
  38. ↑ Locke, MM; Ruth, L S; Millon, LV; Penedo, MC; Murray, JD; Bowling, AT (December 2001). "The cream dilution gene, responsible for the palomino and buckskin coat colours, maps to horse chromosome 21". Animal Genetics. 32 (6): 340–3. doi:10.1046/j.1365-2052.2001.00806.x. PMID   11736803.
  39. ↑ "Color Coat Genetics: Cremello" (PDF). American Quarter Horse Association. Archived from the original (PDF) on January 19, 2016. Retrieved May 29, 2016.
  40. ↑ Cremello & Perlino Educational Association. "The Facts and the Myths". Archived from the original on February 7, 2012. Retrieved December 30, 2008.
  41. ↑ Sponenberg, DP; Bowling, AT (September–October 1985). "Heritable syndrome of skeletal defects in a family of Australian shepherd dogs". The Journal of Heredity. 76 (5): 393–4. PMID   4056374.
  42. ↑ Sellnow, Les (November 1, 2000). "Equine Genetics". The Horse. Retrieved May 18, 2016.
  43. ↑ "Researchers Complete Genome Of The Horse" (PDF). Veterinary Medicine News. Vol. 27, no. 2. UC Davis. Spring 2010. p. 5. Retrieved December 8, 2018.
  44. ↑ "Sequenced horse genome expands understanding of equine, human diseases". Cornell University College of Veterinary Medicine. August 21, 2012. Retrieved April 1, 2013.
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