Nov 10, 2014 | Breeding, Uncategorized
Welcome to part 2 of Equine Coat Color Genetics: Gray, Roan, and Dun
This blog builds on the information presented in the previous blog: Equine Coat Color Part 1. We recommend you read that post first to best understand this one.
The Gray Gene
We all know that gray horses aren’t born gray, but they are not all born black. A gray horse can start out any color at birth, and then they fade as they age, sometimes slowly, and sometimes rapidly. The ‘gray’ gene is simple. ‘G’ stands for ‘gray’, and ‘g’ for ‘NOT gray’.
GG = horse goes gray
Gg = horse goes gray
gg = horse stays whatever color it is at birth
The color that a gray horse is born with is determined by the other color genes. For example:
EE or Ee (black-based), with aa (unrestricted black), with GG or Gg (gray) = Horse born black, then goes gray.
EE or Ee, with AA or Aa (restricted black), with GG or Gg (gray) = Horse born bay, then goes gray.
ee (red-based) with GG or Gg (gray) = Horse born chestnut, then goes gray.
Roaning
The roan gene is a color modifier that causes an intermixing of white hairs with the base coat color, with more white over the neck and body and less white on the head and legs. Black based horses with roan have black and white hairs, and are called blue roans. Chestnut based horses with roan have red and white hairs, and are called red roans. Bay horses with roan have brown and white hairs, and are either called bay roans or strawberry roans.
The roan gene is a dominant trait, meaning that ‘Rn’ for ‘roan’ is dominant to ‘rn’ for ‘NOT roan’. The famous cutting horse mare Royal Blue Boon is an example of a blue roan, and her son, the famous sire Peptoboonsmal, is a red roan.
EE or Ee (black-based), with aa (unrestricted black), with RnRn or Rnrn = Blue Roan
EE or Ee (black-based), with AA or Aa (restricted black), with RnRn or Rnrn = Bay Roan
ee (red-based), with RnRn or Rnrn = Red Roan
Dun Dilution – Dun, Red Dun, and Grulla
The dun gene is a color dilution factor that causes a horse to have a diluted coat color, a dorsal stripe, and other ‘primitive’ markings, such as bars on the legs, and sometimes dark marks near the withers. The dun gene is responsible for grulla, dun, and red dun horses. Dun is a dominant trait. ‘D’ for ‘dun’ is dominant to ‘d’ for ‘NOT dun’. The other color genes determine what shade the base coat color is.
A grulla is a black horse with the dun dilution factor.
EE or Ee (black-based) with aa (unrestricted black) with dd (not dun) = Black.
EE or Ee (black-based) with aa (unrestricted black) with DD or Dd (dun) = Grulla.
A dun is a bay horse with the dun dilution factor.
EE or Ea (black-based), with AA or Aa (restricted black), with dd (not dun) = Bay.
EE or Ea (black-based), with AA or Aa (restricted black), with DD or Dd (dun) = Dun.
A red dun is a chestnut horse with the dun dilution factor.
ee (red-based), with dd (not dun) = Chestnut.
ee (red-based), with DD or Dd (dun) = Red Dun.
Look for the next installment of Equine Coat Color Genetics coming soon for info on Palomino, Buckskin, and Smokey Black!
Oct 2, 2014 | Breeding, Uncategorized
Equine Coat Color Genetics, Part 1: Black, Chestnut, Bay
If I breed a gray mare to a bay stallion, what color will the foal be? If I bred two palominos, how did I end up with a chestnut foal? Equine coat colors actually follow some fairly straightforward rules – in fact, the same ones discovered by Mendel and his infamous peas that you may have learned about in biology. The first thing to understand is that each horse has two complete pairs of chromosomes – one that came from its sire, and the other from its dam. This means it has two copies of every gene, one from mom, and one from dad. The way the two copies of each gene interact with each other, as well as the interaction between separate genes, is the basis for all things genetic, including color.
We use letters to identify which types of each gene (which allele) the horse has inherited. Capital letters identify the dominant allele, and lower case letters stand for a recessive allele. Most of the time, recessive traits or characteristics are only observed if the horse inherits the recessive allele from both parents.
If for example there was a single gene for speed, (there’s not, but for example), then the letters we might use would be ‘F’ for fast, and ‘f’ for slow. If a horse was ‘FF’ (got ‘fast’ from both parents), it would be fast, and if it was ‘ff’, (got ‘slow’ from both parents) if would be slow. But if it was ‘Ff’ (got ‘fast’ from one parent and ‘slow’ from another, then it would still be fast, because ‘fast’, big ‘F’, is dominant to ‘slow’, little ‘f’. The dominant allele trumps the recessive one.
Another way to look at this:
FF = fast horse
Ff = fast horse
ff = slow horse
The ‘extension’ gene: Black, or Red.
The first gene you have to understand when talking about horse colors is the ‘Extension’ gene. Never mind its name, think of this gene as the “black or red” gene. The letters are ‘E’ for black, and ‘e’ for red (chestnut). Black, big ‘E’, is dominant to red, little ‘e’. All horses have this gene, (all horses have every gene), even ones that are colors other than black or chestnut. The other colors exist because of the way other genes interact with the extension gene.
EE = black-based
Ee = black-based
ee = red (chestnut)-based
You might be wondering, if black-based is dominant to red-based, why are there so few black horses compared to bays or chestnuts? Keep reading.
‘Aguti’ makes Bay.
The ‘Aguti’ gene controls black distribution across a horse’s body. Since red-based horses have no black, they will have two copies of this gene, but they won’t play in role in determining the horse’s color. On a black-based horse, the aguti gene determines whether the black will be all over the horse or only on certain parts (like the mane, tail, and legs). There are three alleles for this gene: ‘A’ restricts black distribution the most, (black main, tail and legs only), ‘At’ restricts black a little, and ‘a’ does not restrict black at all.
AA = black restricted to main, tail, legs
Aa = black restricted to main, tail, legs
AtAt = somewhat restricted black
Ata = somewhat restricted black
aa = black is unrestricted, black all over the body
So, combine this with what you know about the extension gene and you get:
EE or Ee (black based) with AA or Aa (restricted black) = Bay horse.
EE or Ee (black based) with AtAt or Ata (some black restriction) = Seal brown horse.
EE or Ee (black based) with aa (unrestricted black) = Black horse.
The reason for few truly black horses is that there are many black-based horses, but most of those turn out bay. Why? Because the big ‘A’, which restricts black, making bay, is dominant to the little ‘a’, and there happen to be a lot more big ‘A’s floating around in the horse population than little ‘a’s.
Remember, the aguti gene does not matter on red-based horses.
It only controls black. So:
ee (red-based) with AA, Aa, or aa (or any combination of aguti alleles) = Chestnut horse.
Sep 26, 2014 | Breeding, Uncategorized
Cloning!
Clones – Where are they now?
I overheard Dr. Bourke talking about cloned horses the other day. Seems like there are a quite a few of them out there now! I’m still not sure that cloning is a good idea, but it was interesting to learn what the cloned horses are up to.
The world’s first cloned horse was born in Italy way back in 2003 – a Haflinger mare that was named Prometea. What’s really interesting is that in this case, the mare that carried the pregnancy was also the mare they took the genetic material from – she gave birth to her own clone!
In 2005, Italy did it again, producing a clone of the famous endurance Arabian stallion Pierez. Then things really took off in 2006 when Texas A&M University announced the birth of FIVE clones of the cutting horse stallion Smart Little Lena. That same year the world’s first commercially cloned horses were born in Oklahoma – copies of top Quarter Horse cutting mares Royal Blue Boon, Tap O Lena, and Playboys Ruby. Since then, there have been handfuls of cloned horses born from several different equestrian disciplines. Examples include show jumping greats ET, Gem Twist, Calvaro V, and Sapphire, dressage stars Jazz and Rusty, international event horses Che Mr. Wiseguy and Tamarillo, barrel racer superstar Scamper, and several other well known cutters including Doc’s Serendipity and Jae Bar Fletch.
Clones Are Reproducing: Prometea is now 11 years old, and in 2008 she had her first foal, a colt, which was reportedly healthy. This was the first offspring of a cloned horse, but there have been several others since. The cloned stallions of Pierez, ET and Gem Twist all have foals on the ground. Pierez is even a grandsire. His first daughter gave birth to a colt in 2012.
Clones for Sale: The Smart Little Lena clones are now 8 years old. One of the five died at the age of 4 from bladder cancer. The remaining four stallions were sold by the syndicate that owned them at the 2009 NCHA World Finals sale. They went for $2400, $3000, $27,000 and $28,000. The highest selling stallion was exported to Australia and now stands at stud for a fee of $1500. One cloned polo pony mount from Argentina sold for a whopping $800,000 in 2010.
Clones in Competition: Because of the high costs involved with producing a clone (roughly $150,000 per horse) it is unlikely that very many will enter competition. The horses being cloned are all from the top ranks of their disciplines, so it would be difficult for the clones to perform as well as the original, let alone surpass or improve on their achievements. Clones have the genetics of superstars, so from a business and breeding standpoint, they have nothing to gain from competition, and everything to lose. For this reason, most clones will be used for breeding purposes.
However, several performance horse organizations have opened the door to allow for cloned animals in competition.
Jan 29, 2014 | Uncategorized
was lounging on the counter the other day, and the whole office was talking about fecals and how important they are and where they fit in a horse’s health care program. I learned from Dr. Lacher (more…)
Apr 22, 2012 | Breeding, Uncategorized
Hay there! The birds, bees, and butterflies seem especially active this week, so I decided another blog on the birds & the bees was appropriate. Last week we introduced the reproductive tract of a mare, its anatomy and function, particularly during the transition into cyclicity. We discussed how the ovary parents the behavior of the uterus and cervix with the presence of large follicles. We introduced that when a large follicle is present, uterine edema (increased water or turgidity) makes thick, welcoming folds, both ready for an egg to come settle in, and an open pathway for sperm to enter through the cervix, and that all of these factors must be present for a mare to be ready for breeding.
The ovary parents the behavior of the uterus and cervix because the of the nature of the hormones being secreted by the various structures on the ovary, and the pattern of blood flow to these structures. These hormones largely change the pattern of blood flow to the uterus, making the layers and folds relatively more or less turgid. Estrogen, which women can thank for most of their complaints in life, increases blood flow to the reproductive tract and relaxes (opens) the cervix – the entrance to the uterus. Estrogen is produced in significant amounts by these magic 35-38mm (dominant) follicles. Whether or not we use deslorelin to help us time ovulation, the follicle ovulates when it is ready, releasing the egg to descend to the uterine horn.
Once the follicle ovulates, which can occur on one or both ovaries, the remaining tissue collapses on itself and begins to transform into another ovarian organ – the corpus luteum (CL). The CL produces the hormone progesterone, which changes the reproductive tract whether or not a breeding and/or pregnancy occurs. Progesterone prepares the uterus for and maintains pregnancy. It reduces uterine edema and closes the cervix tight, so nothing can get in (or out). This is the toned, ‘out of heat’ uterus. We measure progesterone to determine if the mare has reached cyclicity during the spring transition because it will only be produced in significant amounts if the ovary has produced a follicle large enough to ovulate, and result in formation of a CL.
The CL is destroyed by Prostaglandin (I know, it sounds annoyingly similar to progesterone). Prostaglandin is produced by the uterus when no pregnancy is recognized after more than 2 weeks, and during times of inflammation (eg, infection in the uterus). Prostaglandin will only kill the CL once it is mature enough to recognize it – 5 days post-ovulation. This is significant when it comes to ‘short cycling’ a mare. If, for whatever reason, breeding cannot occur this cycle, we can give the horse a shot of prostaglandin (‘prostin’ or Lutalyse) in the muscle to ready the horse for breeding much more quickly. Another time prostaglandin is significant is if a mare double ovulates, and twins occur. If we diagnose twins and crush one for the sake of the other, the inflammation from the act of crushing can result in the loss of both pregnancies.
In review – there are two major ovarian structures, and corresponding hormones, that dictate how the uterus and cervix behave. An egg-containing follicle produces estrogen, which readies the tract for breeding. A corpus luteum (CL), which forms from the ovulated follicle, produces progesterone which readies the tract for pregnancy. Prostaglandin will result in lysis (rupture or death) of the CL, which can result in short-cycling of the mare, or termination of pregnancy. If this summary does not make sense, reread the above blog more slowly.
Don’t forget about our Vaccine Seminar THIS THURSDAY, April 26th at 6 P.M. at the clinic (PLEASE R.S.V.P.!)! We look forward to seeing you there, and don’t forget to come give me some pets! May your litter boxes be clean and your food bowls filled!
Feb 19, 2012 | Uncategorized
Hello there! Hope you are having an enjoyable weekend – I know I am, still cast-free and finally without a limp! A couple weeks ago we offered a cat’s eye view of equine dentistry. This week, I thought it would be important to discuss a little bit further about everything that goes into forming what we call “the anesthetic plan” for your horse’s dental. While your horse is nowhere close to being under general anesthesia, there are anesthetic considerations for every situation involving an equine dental. The first and foremost is safety – for you, the veterinary staff, and your horse. This is the primary reason we ask you to take a step back during your horse’s dental, and let us do the work! Some of the sedatives we use can easily kill a human in fractions of the doses used for the dental, and should only be handled by a veterinarian. The vets are prepared with emergency drugs in case of an accidental overdose or human exposure.
The first thing the Springhill vets do about your horse’s dental happens before your appointment time even arrives. This happens when your horse is already a patient of Springhill Equine, or if you have taken the time to provide complete information about your horse by filling out our new client form and sending it back to us before your appointment (also earning you $5 off your bill!). The vets look at the age, breed, sex, and size of your horse to the best of their ability, and begin to consider what type of sedation would best suit your horse’s physiology. We examine relevant past medical history in our records, and if a dental was performed by Springhill in the past, we consult the last dose used. Between these records, and communication between Dr. Lacher and Dr. King, any past known behavior of the horse (such as needle phobias) or response to sedation (‘He’s a cheap date!’) is taken into account. The doctors arrive on the farm with the foundation of an anesthetic plan in their head – prepared to reconsider our anesthetic approach at every step.
Knowledge of your horse’s behavior is crucial due to another important anesthetic principle called “windup”. Many horses (understandably!) experience anxiety surrounding a dental experience. Stress experienced prior to, during, and in the minutes following sedation causes physiologic responses that can make the horse require more sedation (sometimes A LOT more). We work to minimize that. From the start, we try to move calmly and quietly while sedating the horse, and may give your horse treats to make it a more pleasant experience. Some horses can be very difficult or fearful of intravenous injections, therefore, sometimes more restraint is required to keep everyone involved out of harm’s way. It is important during this time that you let our staff handle the horse. Accidental injection of these drugs into the carotid artery (instead of the jugular vein) will result in the horse experience immediate and profound seizures. We are prepared to deal with these scenarios, however rare. Should this happen, the horse recovers completely with time, except in cases of catastrophic injury. In horses, catastrophic injury is considered a risk with absolutely ANY anesthetic plan – even “acing” your horse for the farrier!
An important part of the anesthetic plan is using the lowest possible dose of each drug, while providing adequate depth of sedation, length of time to complete the dental, and comfort to the horse during the process. Our arsenal contains five main sedatives – xylazine (a.k.a. “Rompun”), Sedivet (romifidine, similar to xylazine), butorphanol (“torb” or Torbugesic), acepromazine (Ace), and detomidine (Dormosedan or “Dorm”). Each of these drugs has its own profile of safety, efficacy and side effects. Before these drugs are even drawn into a syringe for your horse, everything discussed above is considered, as well as an assessment of the horse’s attitude, personality, and comfort level with our presence that day. Environmental factors that may arouse the horse such as wind, temperature, lawn mowers, small children, etc. are also part of the consideration. We listen to the horse’s heart to make sure there are no significant murmurs or arrhythmia’s that could cause an adverse event. Finally, we use the power of synergy to minimize the volume of each drug used by making a cocktail.
I’ll explain by example. When used alone, a whole ml of detomidine may be required to complete a dental on a particular horse. However, Springhill Equine most often uses a triple-threat combination using a “base dose” of xylazine or Sedivet, and add small volumes of the more potent detomidine (Dorm) and Torb. By doing this, we reduce that 1 ml to often 0.2 or 0.3 ml instead. This keeps the dose for this particular drug well within the margin of safety, minimizing its side effects. Likewise for the others in the cocktail (ingredients may vary – e.g. Tennessee Walkers often are better with ace and xylazine cocktails). By using what is termed a “balanced anesthetic technique,” synergy of the sedatives further reduces the required dose. If more sedation is required midway to complete the dental, we try to use the lowest volume of what we feel will be the most effective to finish our work. The next time, we will take into account any “top ups” that were required. The less sedation required for a balanced plane, the more money and time you save!
In summary, there is an enormous amount of thought put into that little syringe that we pull out during your horse’s dental. There are hundreds of thoughts behind it in our doctor’s heads, from possible safety concerns, potential side effects, quality of anesthesia and the plan for next time! If you ever have questions about the sedatives used, you need only ask them and they will happily explain it to you! May your litter box be clean and your food bowl full, until next week!
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