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Arabian Horse Genetics

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allura stevens

on 23 July 2013

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Transcript of Arabian Horse Genetics

One of the oldest known horse breeds.
There is evidence of Arabian- like bones dating back 4500 years.
Originated on the Arabian Peninsula.
It developed as its own breed, it is not a combination of other breeds.
No matter how tall, they are classified as horses.
Breed Characteristics
Head and Face
Dished faces with small, teacup muzzles
Large eyes and nostrils
Broad Forehead
Allows them a larger sinus cavity, letting them breathe easier in their dry, desert place of origin.
Windpipe, throatlatch and neck
Long, arched necks
Large, well- set windpipe on a refined, clean throatlatch
Should be long and fairly level with a naturally high tail carriage.
Only 5 lumbar vertabrae instead of 6
17 pairs of ribs instead of 18
1 less tail vertabrae than other breeds
They are normally 14.2 to 15 hands high, but can be taller or shorter. (there are 4 inches in a hand.)
Breed Overview
When the Arabian first developed, the nomadic Bedouin people favored them.
Because of this, they often shared shared the tents with their owners for shelter from both the environment and theft.
This led to the Arabians having a sweet, willing attitude with a trust towards humans. This would normally be a learned trait, but eventually became an inherited trait in foals, the result of selective breeding.
Cremello, palomino, buckskin/ dun, and sorrel are colors not recognized by the AHA.
Bay, grey, black, chestnut, and rabicano are accepted by the AHA.
Sabino is the only spot pattern recognized by the AHA.
Arabians always have black skin, except under white markings.
Reddish- brown body with black points
Black points are the mane, tail, upper leg, around the muzzle, eyes, and ears
Red bay is when the body color is more of a blood red.
Seal bay is when the body is a very deep brown, almost black with a reddish shade around their flanks, head, and stomach area.
Mahogany bay is just a tad a darker than a seal bay and is most commonly confused with black.
The Agouti gene creates the black points of a bay horse. If it didn't, they'd pretty much just be chestnuts.
Black skin
Mixture of white and dark hairs
Usually born chestnut or a deep bay, starting to turn grey a few days/weeks after being born.
Grey horses can be flea-bitten, which is when they get little spots of red hairs throughout their body.
The rule of genetics for the AHA is that a foal will not turn grey unless one parent is grey.
The entire horse must be black.
They can't have any color other than black anywhere on their body, unless they have a white marking.
Black Arabians are rare; the black gene is recessive to the Agouti gene.
The Agouti gene creates the black points of a bay horse.
This means that both parents must have the black gene, not the Agouti gene, for the foal to be black.
Chestnuts are a coppery color, varying in shade from light golden-red to dark brown.
Dark brown chestnuts are called "liver chestnuts."
Some chestnuts have blonde, or "flaxen" manes and tails.
When foals, chestnuts have blonde hair on their legs which can look like white markings.
The rule of genetics for the AHA is that when two chestnuts are bred, the result will always be a chestnut foal.
Rabicano is a gene that causes a mixture of different colored hairs throughout the body.
Roaning in Arabians is probably just be the effect of sabino or rabicano genes producing white hair on the midsection and flanks.
The rabicano gene is RB and is not completely understood yet.
Sabino is the only spot pattern recognized and accepted by the AHA.
Sabinos have "high white"; white extending above the hocks and knees on the legs.
They also have white spots on their legs, belly and face.
White markings that extend beyond the chin, jaw, and eyes are also characteristics of sabino coloring.
Sabinos can also have lacy or roaned edges on their spots.
An Arabian is considered "maximum sabino" if over 50% of their body is white.
Like the rabicano gene, the sabino gene is not yet fully understood.
The Ideal Arabian
Genetic Disorders
6 known genetic disorders in Arabians.
Two are fatal
Two are disabling and normally end in putting the animal down.
The other two can most normally be treated.
Three are assumed autosomal recessive conditions, which means the flawed gene is not gender related. It also means that both parents have to carry the gene for the foal to receive it.
The other three have so little known about them that the way they are inherited is still to be determined.
Severe Combined Immunodeficiency
Fatal when homozygous
The affected foal is born with no immune system, generally dying within 5 months of birth from an infection.
To prevent a foal being born with SCID there is now a DNA test that can be performed on healthy horses to see if they carry the gene.
Cerebellar Abiotrophy (CA or CCA)
Homozygous horses are affected
Carriers show no signs
Affected foal starts to show signs after about 6 weeks, if it is severe.
They have head tremors, a wide stance, and severe incoordination.
These symptoms are related to the death of purkinje cells, which are in a part of the brain called the cerebellum.
The level of intensity varies, some foals show symptoms immediately but others may live their whole life before they are diagnosed.
Occipital Atlanto-Axial Malformation (OAAM)
The cervical vertebrae fuse together at the neck and base of skull. (Axis to Atlas and Atlas to skull)
Symptoms can range from mild incoordination to the paralysis of the front and even hind legs.
Some affected foals can't even stand to nurse while others don't show symptoms for several weeks.
It is the only cervical spinal cord disease observed in horses under 1 month of age.
A radiograph can diagnose the condition although there is no genetic test for OAAM.
The hereditary component is not well researched at present.
Equine Juvenile Epilepsy or Juvenile Idiopathic Epilepsy
Not usually fatal
Foals seem normal inbetween seizures
Seizures normally stop between 12 and 18 months of age
Seizure medication can be given to help reduce the severity of the seizures
The condition has been studied since 1985 by the University of California, Davis.
Although all the cases studied were of one bloodline group, the genetic mode of inheritance is unkown.
Guttural Pouch Tympany (GPT)
Can occur in horses from birth to 1 year
More common in fillies than colts
Thought to be genetic in Arabians, maybe even polygenic in inheritance, but more study is needed to be certain.
Affected foals are born with a defect that only allows air to get in, not out. (Technically speaking the pharyngeal opening of the eustachian tube acts like a one way valve.)
The affected guttural pouch becomes expanded with air and swellls.
Breathing in affected horses is noisy
Signs and a radiograph examination of the skull can diagnose this disorder.
Antimicrobial therapy can treat respiratory inflammation.
Surgery is needed to correct the malformated guttural pouch and provide a route for air.
Successfully treated foals can grow up to live useful lives.
The inheritance of white facial markings is multifactorial
Hypothesis states that the number of cumulative alleles influences the variation of the white face markings.
The amount of white correlates with the number of genes
Interacting nongenetic factors also influence the variation
For the study, the facial region was divided into five sections and each horse was given a score according to the regions with white markings.
The study included twenty two sire families, each sire family consisting of a sire, his foals, and the foals' dams.
A heritability study showed that about 2/3 of the different phenotypes in white facial markings among Arabians is thanks to genetic differences.
Bloody Shouldered Greys
Large area of flea bites
Can get bigger as the horse grows older
Lavender Foal Syndrome (LFS) A.K.A
Coat Color Dilution Lethal (CCDL)
Fatal when homozygous
Carriers of the gene show no signs
Affected foals are born with a diluted coat color, the ends and occassionally the whole hair being lightened.
They cannot stand at birth, often have seizures, and are more often than not put down within few days of birth.
Fri. Dec. 16th
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Thurs. Jan. 5th
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Facial Markings
B b
b Bb bb
Punnet Square to show the relationship between the Agouti gene and black gene.
B= Agouti gene b= black gene
These pictures show an example of our horses
supporting the hypothesis.
Rithlior's facial marking was 3/4 in length and
had a small dip near the right side.
Goldy's mark was full in length and also had a dip in the right
Sylvia and Lea, the children of Rith and Goldy,
both had full blazes with dips in the right side.
This supports the hypothesis that Arabian face markings
can be genetically inherited.
Goldy and Sylvia
Sylvia and Lea
Greying process of our mare Lacy
16 years
2-3 years
Full transcript