HRG-003

TEXAS A&M UNIVERSITY

DEPARTMENT OF ANIMAL SCIENCE
EQUINE SCIENCES PROGRAM

THE GENETICS OF EQUINE COAT COLOR

D. Douglas Householder

INTRODUCTION coat color. Early research in this area dealt

exclusively with analysis of stud books,
History observation of various matings with subsequent
color foals produced, and then hypothesizing
Great variation is present in horses of which genes were involved. Inaccurate records,
today. There are large horses and small horses, foals changing colors, and lack of common color
riding horses and driving horses, draft horses and descriptions among horsemen were also problems.
race horses. There is, no doubt, a type of horse for Since the early 1940's; however, geneticists have
almost every possible purpose. Although type and drawn on the more exacting information obtained
performance ability are quite variable, they are not from planned experimentation with laboratory
more variable than the colors of the horses. mammals. The close relationship is now evident
and as a result many questions on equine color
The ancestors of the domesticated horse can now be answered with reasonable certainty.
did not vary much in color, but were chiefly of
"wild type" coloration. This color was of great Genetics
value in hiding these wild horses from their
natural enemies. This concealing type of Inside the cells of all animals are found
coloration can still be seen in the few Przewalkski chromosomes and genes. Chromosomes are paired
horses, undomesticated and near extinction in thread-like structures which carry the genes. Each
Mongolia in Central Asia. When some of these body cell contains a certain number of pairs of
horses were domesticated some 4,000 years ago, it chromosomes (eg. horse - 32, man - 23). Genes
is probable that some varying colors were are the units of inheritance which dictate what an
preferred in selection and breeding. This breeding individual will look like. This outward expression,
by color may have brought together some of the called phenotype, is a result of an animal's genetic
recessive genes, eventually resulting in different makeup, called genotype. As chromosomes occur
colored horses. Also, through the ages, mutations in pairs, so do genes. Two genes exist side by side,
in these basic genes probably played a role in each on one of the chromosomes of a pair. An
development of different colors. allele is one member of this pair of genes, or a
partner gene. The specific position, where paired
Ancient paintings and writings suggest genes are found, is called their loci.
that color in horses has been variable for
sometime. Spotted horses may have been present The genotype of a chestnut colored horse,
as early as 1400-1300 B. C. as Egyptian tomb in this example, is written as
paintings showed two horses so colored. In the AabbCCddEEggrrssww where each pair of letters
Bible (Rev. 6) symbolic white, red, black and pale represents a pair of genes at a loci. Note within
colored horses are mentioned. the pairs some genes are written with a capital
letter; some with small letters. A capital letter
means that particular gene is a strong or dominant
Today there is disagreement among the gene while a small letter represents a weak or
experts on many aspects of the genetics of equine recessive gene. Within the gene pairs within a
genotype, three combinations are possible. There of palominos (Cccr), buckskins (Cccr), duns (Cccr),
may be two dominant genes (EE), a dominant and cremellos (ccrccr), and perlinos (ccrccr) ;however, no
a recessive gene, or two recessive genes. Usually conclusive evidence was presented. Singleton and
when two dominant genes are present the second Bond (1966) adapted this ccr mutant theory to
dominant one adds nothing. Exceptions to this are explain diluted colors in place of the dominant
known though where two dominant genes are dilution theory forwarded by Castle (1947).
twice as potent as one dominant gene. When a Singleton and Bond (1966) includes this proposed
dominant and a recessive gene are present within ccr allele in writing horse genotypes.
a pair, two expressions are possible. One, the
dominant gene is dominant over the recessive B Series
gene, called complete dominance; or two, the two
express themselves in an intermediate fashion, In the horse, as other mammals, gene B
called incomplete dominance. Lastly, two is responsible for the production of black pigment.
recessive genes together either add nothing to the Theoretically if no modifier genes affected the
phenotype or express themselves differently. intensity or distribution of black pigment, all
Within a given genotype, several pairs of genes black horses (BB or Bb) would be the same color.
work in combination to produce the animals' This is not the case. According to Salisbury
phenotype. Usually certain genes modify only (1941), some horses are foaled jet black and hold
slightly the expression of other genes; however in their color, while other horses, are foaled a mouse-
some cases, one gene completely dominates all brown-gray, are black when kept stalled, but fade
other genes. This is called epistasis. either to brown or red in intense sunlight. Some
horses have localized black pigmentation in the
BASIC COLOR GENES extremities. Examples are bays, some browns,
buckskins, duns, grullas, and perlinos. In both of
C Series these cases where black is changed, modifier
genes (A, E and/or D) are operating in the
The presence of eumelanin (black-brown) genotype.
and/or phaeomelanin (red-yellow) pigments cause
skin, coat and eye color in mammals. When gene Gene b, a recessive mutant of gene B,
C is present, normal pigment formation reactions produces a rich brown pigmentation; therefore,
occur; however, mutants of gene C result in horses with genotype bb are chocolate brown
complete or partial albinism. In complete albinism colored called chestnut. This rich brown color is
(cc), no pigment is formed. The hair is white, the different than the straight brown color resulting
skin is pink and the eyes are red, due to the visible from the action of the at allele in the agouti series
color of the blood. Some familiar examples of (Searle, 1968). As is true with gene B, gene b is
complete albinos are white rabbits, rats, and mice. modified by the action of genes A, E and/or D.
In some incomplete albinism cases, the skin, coat Their pigment diluting, restricting and/or
and eye colors are the result of the actions of such extending actions, in conjunction with the bb
gene C mutants as cch or cH. Mammals carrying genes, modifies chestnuts to certain types of
these mutations are the Chinchilla rabbit (cchcch) browns, sorrels, claybank duns, palominos and
and the Himalayan rabbit (cHcH). cremellos.

Horse researchers are in general

agreement that a dominant gene C is responsible A Series
for presence of pigment in the skin, coat and eyes.
Consequently, gene C is usually omitted when Gene A acts in conjunction with genes C
writing horse genotypes. Horsemen often refer to and B to produce a concealing coat pattern known
horses with light colored skin, hair and partially as agouti or "wild type". The characteristics of this
or totally pigmented eyes as albinos; however, coat pattern are black pigment on the dorsal and
according to Searle (1968), no well authenticated peripheral parts of the body and to particular parts
case of complete albinism has ever been reported of the individual hairs. Familiar examples are the
in the equine. The only gene C mutant proposed cottontail rabbit and the wolf. Loss of the wild
in the horse was that of ccr (Odriozola,1951). He pattern results when gene A mutates to recessive
postulated this allele was responsible for the color gene a. In homozygous form (aa), this gene pair
causes an individual to be uniform in color. In in bay offspring. Further investigation is needed in
rabbits, rodents and dogs, gene A has also this situation.
undergone a second mutation to gene at. When
homozygous (atat), this genotype causes black and Generally, geneticists have considered
tan coloration. Traces of the agouti are still the various colors of duns (ABED) to be the result
evident; however, in this pattern. of the wild pattern A gene in combination with the
D and B genes. After the hypothesis of a possible
Gene A, dominant to a, in horses is mutant, at, Castle and Singleton (1961) stated that
responsible for bodies of one color and manes and the red or claybank dun, possessing a yellowish-
tails of another. This wild type pattern was first brown body color with a dark spiral stripe, bars on
noted in the Przewalski horses, the the legs and/or both, most likely carries an at, not
undomesticated ancestor to modern horses. an A gene. The darker extremities in the
Phenotypically this horse's body color is neutral claybank dun (atbbeeDd), as compared with the
gray (mixed yellow and black pigments) with a palomino (AbbeeDd), are due to the presence of
blackish mane and tail, blackish legs, and a dorsal the at gene, according to these authors.
stripe (Castle, 1953). Castle and Singleton (1961)
reported seeing horses with similar color on the E Series
Argentina Pampas. According to Castle and
Singleton (1961), the wild type pattern is seen In the horse, as in many other mammals,
today in some domestic varieties. Examples are genes E, e and ED are present. Although three
bays, buckskins, duns, grullas, perlinos, alleles are known to be present in this series, an
palominos and sorrels with light manes and tails. individual can possess only two of them. Gene E
The latter two have lighter manes and tails than permits black-brown pigment to be normally
bodies due to the action of another gene on dark extended uniformly throughout the coat in the
pigment, after it is concentrated in the manes and absence of A. In the presence of A, the degree of
tails. All, however, have gene A in their extension is decreased. Examples are the uniform
genotypes. liver chestnut (aabbE) and the chestnut (AbbE),
respectively.
Three alleles of gene A have been
reported in the horse. According to Searle (1968), Gene e is postulated to be a mutant
the non-agouti allele, a, leads to absence of yellow recessive allele of gene E. In the recessive
pigmentation in the body. Horses of the genotype homozygous form, gene e restricts the distribution
(aa) are uniformly dark. For example, in a dark of black-brown body pigmentation in a similar
bay (ABE), substitution of the non-agouti alleles manner to that of gene A; however, it does not
would render an individual uniform or recessive form the concealing pattern of gene A. A genotype
black (aaBE). Substitution of non-agouti alleles containing genes ee and gene A is characterized
for the agouti allele, in horses with bb in their by black-brown pigment in the mane, tail and legs
genotype, produces uniform chestnut or sorrel while the central body coat remains almost
coloration. completely devoid of black-brown pigment. In its
place, red-yellow pigments form. Castle (1953)
Odriozola (1951) and Castle and points to the typical red or blood bay (ABee) horse
Singleton (1961) postulated the presence of an A+ as an example of this recessive red mutation. This
allele in the horse. They believe the striped agouti color bay's general body color is red, not a mixture
pattern (bars on legs, dorsal stripe, etc.) of wild of black and yellow pigments as in the Przewalski
horses and certain domestic breeds is caused by a horse (ABE). Both however, have black manes,
dominant allele A+. In addition, Castle and tails, and legs resulting from the primitive A
Singleton (1961) postulated an A+ allele to be pattern gene.
responsible for brown, black-brown or seal brown
color where the mane, tail, feet and legs are black If gene A is absent, ee leads to a horse
and the body is brown to black with traces of light with a more uniform color; however, somewhat
areas on the muzzle, neck and flanks. They stated more reddish in the body. An example is the
this allele is dominant over non-agouti and recessive black horse (aaBee) with a slightly
recessive to gene A; however, Searle (1968) stated darker mane and tail than the central body. When
that brown x black matings quite frequently result exposed to intense sunlight, this color fades to a
redder color. (AbbEDD). This dilute horse's phenotype is an
ivory white coat with a lighter mane and tail and
Salisbury (1941) reported that some black pink skin. This horse is called a cremello or a type
horses were foaled a peculiar mouse-brown-gray A albino. Mating two buckskin horses, the
color and that they faded to a red color when offspring would be one bay, two buckskins and
exposed to the sunlight. Other black horses, he one individual with a cream colored body and a
stated, were foaled jet black and remained so even darker mane and tail, resulting from gene B. This
when exposed to intense sunlight. According to individual is called a perlino or type B albino with
Castle (1953), the former is genotypically a genotype ABEDD. Note the only difference in the
recessive black while the latter is a dominant genotypes of these two horses is that the cremello
black. Dominant black was first postulated in is a diluted chestnut while the perlino is a diluted
rabbits (Punnett, 1912) and is common in black.
Shetland ponies. The gene responsible is ED which
increases the amount and distribution of black OTHER COLOR GENES
pigment in any coat. In addition, in some cases, it
can even mask the presence of gene A. This Gene W
explains how a black stallion (ABCEDE) mated to
a black mare (aaBEE) will occasionally produce a The white horse has pink skin, white coat
bay foal. hair, a white mane and tail, white hooves and
always colored eyes, either brown, blue or hazel.
D Series Only occasionally are small pigmented areas
found in the skin or hooves. Cream, ivory and
Much controversy exists with regard to gray colored horses are often confused with the
gene D for dilution. Early researchers referred to dominant white horse; however, the former two do
it as a dominant dilution gene, but according to not have snow white coats, white mane and tail
Singleton and Bond (1966), gene D is not really hairs and the latter does not have pink skin or
completely dominant since the phenotype of the white hooves.
heterozygote (Dd) is halfway between those of the
two homozygous forms (DD and dd). Wriedt (1925) stated that white in horses
was caused by recessive characters; however, most
In heterozygous form, gene D results in researchers are now in agreement that dominant
moderate reduction in the intensity of all gene W, epistatic to all coat colors, is responsible
pigmentation whether black, brown, red or yellow. for this white phenotype. The ww genotype allows
For example, gene D dilutes a mahogany bay normal expression of the other genes in the
(ABEdd) to a dun (ABEDd), a red blood bay genotype. Castle (1953) stated that no true
(ABddee) to at buckskin (ABDee),a recessive breeding white stallion had ever been reported,
black (aaBddee) to a grulla (atBDdE), and a seal suggesting the WW genotype to be a lethal
brown (atBddE) to a light seal brown (atBDdE). condition. Pulos and Hutt (1969),after 15 years of
According to Castle and Singleton (1961), the mating white horses, confirmed this stating that
effect of gene D on brown pigment seems greater the WW individual dies during early embryonic
than on black; therefore, a chestnut (AbbEdd) development. This WW genotype is also lethal in
becomes a palomino (AbbDdE) with a white mane Dexter cattle, platinum foxes, bluefrost minks and
and tail and a yellowish-brown body color. certain mammals, according to Searle (1968).
According to Castle and King (1951), Castle and
Singleton (1961), and Singleton and Bond (1966), Two additional alleles of the W gene, W1
2
the D gene has little diluting effect in the absence and W , have been proposed by Miller (1969) to
of gene A. be involved in the complex genetics of Appaloosa
coat inheritance. He stated individuals of the W1
In homozygous form (DD) the dilution W1 or W1w genotypes would exhibit Appaloosa
gene causes a much greater reduction in the type while those of W2W2 or W2w genotypes
intensity of pigmentation. For example, when would be of ranger type.
mating a palomino with a palomino, the offspring,
on the average, will be one full colored chestnut, Gene G
two palominos and one very dilute individual
 The graying gene, gene G, prevents Castle (1953) has referred to roaning as
melanin granules from passing into the body "non-progressive" silvering to distinguish it from
hairs. Thus horses turn gray with increasing age. graying or progressive silvering. Foals carrying
Gray horses are born with a solid color coat, but the Rr genotype are born roan and the number of
upon loosing this juvenile coat, white hairs begin white hairs remain substantially unchanged
to appear. At this stage gray horses are often throughout life. This is in contrast to gray foals
confused with roans. According to Salisbury who are born a basic color then white hairs appear
(1941), the rate at which a foal will gray out later and increase in number throughout life.
depends on his genotype; with homozygous Castle (1953) states also that red roans are more
dominant (GG) individuals graying sooner than common than blue roans.
heterozygotes (Gg). This has not been confirmed
by other authors. Castle (1953) stated that some Although the genetics of Appaloosa coat
horses are completely gray at four years of age color are still unknown, Miller (1969) suggests the
while others require up to 12 years of age before possibility that certain Appaloosa color patterns
completely graying. He called, this graying are the result of non-progressive silvering in
process "progressive silvering". which white hairs are localized more or less
completely in large patches on the rump.
Well authenticated cases have been
reported where gray stallions produce all gray Genes for Appaloosa
offspring; therefore, horses with GG and Gg
genotypes are gray (Castle, 1953). Gray is Appaloosa coat color inheritance is
dominant over all colors except white; therefore, complex as is suggested by the fact that many
only gray horses produce gray offspring. different types of Appaloosa patterns occur.
Although, dapples are common among gray Examples are frost, leopard, marble, snowflake,
horses, not all grays are dappled. According to spotted blanket, white blanket patterns, etc. While
Wriedt (1925) dappling is caused by another several authors have referred to Appaloosa
independent gene. patterns, only Miller (1969) has conducted a
detailed study and forwarded a possible hypothesis
It is interesting to note that gene G has as to the genotypes of these Appaloosa
an unfavorable pleiotropic effect, for gray horses phenotypes. It is as follows:
are exceptionally prone to skin cancers in the form
of melanomas (Searle, 1968). Freckling is The basic expression of the Appaloosa
common in old white horses and seems to be color pattern is controlled by a single gene (Ap),
associated with melanomas in the perianal region. which is apparently dominant. When this gene is
present the color pattern can be expressed,
Gene G is present to some extent in all providing modifying genes are also present. A
breeds of horses; however, it is most common series of modifying genes control the expression of
among Arabians, Lippizaners and Percherons white and another series control the expression of
(Castle and Smith 1953). In some color breeds, spots. Horses with the Ap gene will have white
gene G is detrimental. Hatley (1962),warned that distribution if modifying genes are present which
Appaloosa breeders should avoid the graying prevent pigment formation. Inasmuch as the
gene, "the gene that kills Appaloosa color." distribution of white radiates both anteriorly and
posteriorly from the sacral (hip) area, the
Gene R modifying genes work as a series. It may be that if
one or two modifying genes are present, the horse
Roan color in horses is defined as white will lack pigment in the sacral areas; if three or
hairs intermingled with black, brown, red or four modifiers are present a slightly larger area
yellow hairs in the coat. Individuals of Rr will be white, etc., up to the all white horse. Thus,
genotype are roan while rr individuals exhibit the modifying genes would be quantitative in
normal coloration with no roaning. Castle (1953) nature. A horse with the Ap gene, but with no
stated that no true breeding roan horse has been modifiers, or a horse with modifiers but not the
reported, suggesting the RR genotype as was WW, Ap gene, would not show white distribution.
is lethal.
The modifiers cannot express themselves
except ln the presence of the Ap gene. It is of ss
possible one pair of recessive genes (ww) must be
present to allow expression of the white modifiers. Ap - ww ss - blanket with spots
This would explain how a non-blanketed
Appaloosa (Ww) would produce blanketed Ap - ww Ss - blanket, no spots could produce
offspring when the other parent was non- spots
Appaloosa.
Ap - Ww ss - no blanket with spots, could
A series of genes for spotting also served produce blanket
as modifiers of the Ap gene. They are exhibited in
horses with or without the white modifiers and Ap - Ww Ss - no blanket, no spots, could produce
they appear to be independent of the white blanket and spots
modifiers in their mode of inheritance.
Modifying genes must be present in each
Physiologically, they inhibit the white of the above four genotypes if blanket or spots are
modifiers and allow the production of pigment in exhibited. Size of the blanket and the number of
spots. The entire white area may be spotted or spots would be determined by the number of
only a portion. The expression of these genes modifying genes present.
tends to begin in the sacral area and radiate both
anteriorly and posteriorly. However, this tendency Studies would indicate that the
was not nearly so marked as with the expression expression of white and spots are sex influenced.
of white. Some horses had spots in widely It may be that the genes for white and spots act in
scattered areas. Modifying genes for white and following manner:
spots may be present in solid colored horses.
Males Females
Blanketed horses with no spots, when
mated, can produce spotted offspring. The same is WW Solid Solid
true if one parent is blanketed with no spots and Ww White Solid
one is solid color. Evidence that the action of ww White White
spotting genes is not dependent upon the presence SS No Spots No Spots
of the white modifiers, is furnished by the fact that Ss Spots No Spots
solid colored horses with the Ap gene can be ss Spots Spots
spotted.
The roan gene may act in the following
As with the white modifiers, the spotting manner:
genes may be controlled by a single pair of
recessive genes (ss), which in the presence of the Males Females
Ap gene allow the expression of a series of
modifiers for spots. Thus, horses with blankets RR Roan Roan
and no spots could produce spots. Rr * Roan
rr non-roan non-roan
A model of the color inheritance could be
*
as follows: This genotype may be expressed in the
male as fringe roaning around the blanket
Ap - expression of Appaloosa color

ww - expression of white color Genes for Spotting

w1w1, w2w2, etc. - modifiers of Ap acting in the The genetics of white spotting in horses
presence of ww has not been worked out. Several spotting genes
have been hypothesized by researchers. In most
ss - expression of spots cases, researchers have; however, recognized that
spotted horses are of two distinctly different
s1s1, s2s2, - modifiers of Ap acting in the presence phenotypes.
 Castle (1954) said spotting is caused by
gene P (for piebald or pinto) which only expresses
itself when in heterozygous (Pp) condition. Lasley
(1970) stated that dominant gene S causes white
spotting. In addition he added that horses of
genotype SS or Ss were spotted while those with
ss genotype were full colored. Jones and Bogart
(1971) postulated gene T (for tobiano) was
responsible for dominant white spotting patterns.
These authors also hypothesized that several
modifier genes operated in conjunction with the T
gene to cause variable white markings on the face,
body, feet and legs.

Brown (1970) also referred to a dominant

gene T, stating that homozygous recessive (tt)
horses were solid colored while heterozygotes (Tt)
were spotted. He also stated that since all other
pattern genes seem to have harmful effects in the
homozygous condition, it would be unusual if
animals of TT genotype are unaffected. According
to Brown, cases have been reported where two
solid colored horses have produced tobiano
offspring, suggesting the heterozygote may not
always show white spotting.

Concerning recessive spotting, Kremols

(1933) coined the term splashed white to describe
the ventral lack of pigmentation of this recessive
pattern. Castle (1940) postulated that a recessive
factor was responsible for minor white spotting on
the face, legs and feet and that in its maximum
expression, white spotting would be found on the
main part of the body. Jones and Bogart (1971)
stated that modifier genes caused the variability in
splashed white patterns. They called this
phenotype overo and stated it was the result of
gene O in homozygous recessive (oo) form.
According to Brown (1970), gene O in
heterozygous form (Oo) allows normal expression
of the other genes in the genotype.

A problem of serious nature that the

overo breeder faces is the fatal white foal,
according to Irving (1971). This foal is produced
approximately 10% of the time in overo x overo
matings or in matings of two individuals with
overo genes in their genotype. The foal from these
type matings usually dies within 5 days after birth.
The causes of death in this abnormal foal are an
atretic color and/or an abnormal blood factor
similar to erythroblastosis in humans.
 GENOTYPES AND PHENOTYPES

The genotypes listed below were obtained from Castle and Singleton (1961) and Lasley (1968). For
genotype simplification, gene C, as well as other non-expressing gene pairs, have been omitted. Also
dominant genes alone mean that the allele could be either dominant or recessive without changing the
individual's phenotype.

COLOR GENOTYPE PHENOTYPE

Black aaBE Recessive black, uniform

aaBee Recessive (smokey) black, dark mane and
tail
ABED Dominant (jet) black

Chestnut AbbE Chestnut, dark mane and tail

aabbE Liver chestnut, uniform
aabbEDd Light chestnut, uniform

Sorrel aabbee Sorrel, uniform

Abbee Sorrel, light mane and tail
aabbeeDd Light sorrel, uniform

Bay ABE Ancestral bay

ABE Mahogany (dark) bay
Abee Blood (red) bay

Brown atBE Seal brown, light points

atBee Seal brown, light points inconspicuous
atbbE Chestnut "brown"
atbbee Sorrel "brown"
atBEDd Light seal brown
atBeeDd Light seal brown

Dun ABED Dun

atbbEDd Clay bank dun, yellow-brown body, mane
and tail
atbbeeDd Clay bank dun, yellow-brown body, dark
mane and tail

Buckskin ABeeDd Buckskin, clear yellow body color

aaBbEDd Crypto-buckskin, dark cream body, mane
and tail
ABEDd Sooty buckskin, black mane and tail

Dilute Black aaBEDd Dilute mouse, black, uniform

aaBeeDd Dilute mouse, black, mane and tail
Palomino abbeeDd Palomino, clear golden body, white mane and
tail
AbbEDd Palomino, sooty red body, white mane and
tail
aabbEDd Palomino, sooty red body, mane and tail
aabbeeDd Palomino, clear golden body, mane and tail

Cremello AbbEDD Cremello, ivory coat, light mane and tail

Perlino ABEDD Perlino, cream body, straw colored mane and

tail

Dominant Ww White
White ww White not expressed

Gray GG Gray after first shedding

Gg Gray after first shedding
gg Gray not expressed

Roan ABER Red roan, dark mane and tail

aaBER Blue roan
AbbeeRr Strawberry roan, light mane and tail

SAMPLE MATINGS

Working crosses with several pairs of coat color genes is not as complicated as it first appears. This
is because many times individuals mated are homozygous for the same genes. Each time a pair of genes is
homozygous the same way in both parents those parents can produce only that genotype of offspring. On the
other hand, when the parents are different in one or more pairs of genes, one to several different offspring
genotypes are possible. The more pairs of genes for which parents are different, the more difficult the genetic
combinations. For illustration, below are examples of four sample matings:

Example 1. Parents: aabbddeeggrrssww aabbddeeggrrssww

Sorrel(female), uniform Sorrel(male), uniform

Genetic Combinations: Both parents have exactly the same genotype; therefore only one combination is
possible.

Offspring: 100% aabbddeeggrrssww sorrels, uniform

In the next 3, more complex examples, examine the genotypes of each parent, noting those specific
gene pairs which are not homozygous the same way in both parents. From these, list all possible combinations
of genes contributed by the mare to the left of the box. Do likewise for the stallion and list at the top of the
box. Fill in offspring squares with the approximate gene combinations. Figure the percentage of each
genotype.
Example 2. Parents: A1a2bbddeeggrrssww A1a2bbddeeggrrssww
Sorrel(female), Sorrel(male),
light mane and tail light mane and tail

Genetic Combinations:
(male)

A1 a2

A1 AA Aa
(female)
a2 Aa aa

Offspring: 25% AAbbddeeggrrssww sorrel, light mane and tail

50% Aabbddeeggrrssww sorrel, light mane and tail
25% aabbddeeggrrssww sorrel, uniform

Example 3. Parents: a1a2B1b2ddEEggrrssww A1a2b1b2ddEEggrrssww

Black(female), uniform Chestnut (male),
dark mane and tail
Genetic Combinations :
(male)

A1b1 A1b2 a2b1 a2b2

a1B1 AabB AabB aabB aabB

a1b2 Aabb Aabb aabb aabb

(female)
a2B1 AabB AabB aabB aabB

a2b2 Aabb Aabb aabb aabb

Offspring: 25% aabBddEEggrrssww black, uniform

25% AabBddEEggrrssww bay, mahogany
25% AabbddEEggrrssww chestnut, dark mane and tail
25% aabbddEEggrrssww chestnut, uniform

Example 4. Parents: AAbbD1D2E1E2ggrrssww AAbbd1d2e1e2ggrrssww

Cremello (female) sorrel (male) light mane and tail
Genetic Combinations:
(male)

d1e1 d1e2 d2e1 d2e2

D1E1 dDeE dDeE dDeE dDeE

D1E2 dDeE dDeE dDee dDee

(female)
D2E1 dDeE dDeE dDeE dDeE

D2E2 dDeE dDeE dDeE dDeE

Offspring: 100% AAbbDdEeggrrssww palominos

 SELECTED REFERENCES

Brown, J. 1970. Color Inheritance in Horses. The Inheritance. Appaloosa Horse Club, Inc.,
Paint Horse Journ., May-June. Moscow, Idaho.

Castle, W. E. 1940. The genetics of coat color in Odriozola, M. 1951. A Los Colores Del Caballo.
horses. Jour. Hered. 31: 127. Madrid.

Castle, W. E. 1946. Genetics of the palomino Pulos, W. L. and F. B. Hutt. 1969. Lethal
horse. Jour. Hered. 37: 35. dominant white in horses. Jour. Hered.
60: 59.
Castle, W. E. 1948. The abc's of color inheritance
in horses. Genetics 33: 22. Punnett, R. C. 1912. Inheritance of coat color in
rabbits. Jour. Genetics 2: 221.
Castle, W. E. 1953. Coat color inheritance in
horses and other mammals. Genetics 39: Salisbury, G. W. 1941. The inheritance of equine
35. coat color, the basic color patterns. Jour.
Hered. 32: 235.
Castle, W. E. 1961. Genetics of the claybank dun
horse. Jour. Hered. 52: 121. Searle, A. G. 1968. Comparative Genetics of Coat
Color In Mammals. Academic Press Inc.,
Castle, W. E. and F. L. King. 1951. New evidence New York and London.
on the genetics of the Palomino horse.
Jour. Hered. 42: 60. Singleton, W. R. ant Q. C. Bond. 1966. A allele
necessary for dilute coat color in horses.
Castle, W. E. and W. Singleton. 1961. The Jour. Hered. 57: 74.
palomino horse. Genetics 46: 1143.
Wreidt, C. 1925. Color sided cattle. Jour. Hered.
Castle, W. E. and F. H. Smith. 1953. Silver 16: 51.
dapple, a unique color variety among
Shetland ponies. Jour. Hered. 44: 139- Wright, S. 1917. Color inheritance in mammals.
145. Jour. Hered. 8: 561.

Gremmel, Fred. 1939. Coat color in horses. Jour.

Hered. 30: 437.

Hatley, G. B. 1962. Crosses that kill your color.

Appaloosa News, Feb.

Irving, W. M. 1971. Genetics at work. Paint

Horse Jour., Jan.

Jones, W. E. and R. Bogart. 1971. Genetics of the

Horse. Caballus Publishers; East
Lansing, Michigan.

Kremola, V. 1933. The pied and splashed white

patterns in horses and ponies. Jour.
Hered. 24: 65.

Lasley, J. F. 1970. Genetic principles in horse

breeding. The Quarter Horse Journ., Jan.

Miller, R. W. 1969. Appaloosa Coat Color

NOTES