Primary Lens Luxation (PLL) is a well-recognised, painful and blinding inherited eye condition that affects many breeds of dog, particularly terrier and terrier-type breeds including (but not restricted to) Miniature bull terriers, Tibetan terriers, Jack and Parson Russell terriers, Lancashire Heelers and Chinese Crested dogs, also the Australian Cattle Dog, Jagd Terrier, Patterdale Terrier, Rat Terrier, Sealyham Terrier, Tenterfield Terrier, Toy Fox Terrier, Volpino Italiano, Welsh Terrier, Wire-haired Fox Terrier and Yorkshire Terrier.

In affected dogs the zonular fibres which support the lens breakdown or disintegrate, causing the lens to fall into the wrong position within the eye. If the lens falls into the anterior chamber of the eye glaucoma and loss of vision can quickly result.

Scientists at the AHT have identified a mutation that is associated with the development of PLL in several breeds of dog. The DNA test we are now offering examines the DNA from each dog being tested for the presence or absence of this precise mutation. It is thus a ‘mutation-based test’ and not a ‘linkage-based test’

Breeders will be sent results identifying their dog as belonging to one of three categories:
CLEAR: these dogs have two normal copies of DNA. Our research has demonstrated clear dogs will not develop PLL as a result of the mutation we are testing for, although we cannot exclude the possibility they might develop PLL due to other causes, such as trauma or the effects of other, unidentified mutations.

CARRIER: these dogs have one copy of the mutation and one normal copy of DNA. Our research has demonstrated that carriers have a very low risk of developing PLL. The majority of carriers do not develop PLL during their lives but a small percentage do. We currently estimate that between 2% – 20% of carriers will develop the condition, although we believe the true percentage is nearer to 2% than 20%. We do not currently know why some carriers develop the condition whereas the majority do not, and we advise that all carriers have their eyes examined by a veterinary ophthalmologist every 6- 12 months, from the age of 2, throughout their entire lives.

GENETICALLY AFFECTED: these dogs have two copies of the mutation and will almost certainly develop PLL during their lifetime. We advise that all genetically affected dogs have their eyes examined by a veterinary ophthalmologist every 6 months, from the age of 18 months, so the clinical signs of PLL are detected as early as possible.

Breeding Advice
Our research has also demonstrated that the frequency of the PLL mutation is extremely high in the PLL-affected breeds that we have studied in depth. This means that allowing only CLEAR dogs to breed could have a devastating effect on breed diversity and substantially increase the likelihood of new inherited diseases emerging. Therefore, we strongly advise breeders to consider all their dogs for breeding, regardless of their PLL genotype. GENETICALLY AFFECTED and CARRIER dogs can be bred with, but should only be bred to DNA tested, CLEAR dogs. All puppies from any litter that has at least one CARRIER parent should be DNA tested, so that the CARRIERS can be identified and followed clinically throughout their lives. This practise should be followed for at least one or two generations, to allow the PLL mutation to be slowly eliminated from the population without severely reducing the genetic diversity of breeds at risk.

Frequently Asked Questions. If you have any questions about the PLL test please see if you can find an answer in our list of FAQ’s on our website PLL Genetics

Samples submitted should be cheek swabs ( a non-invasive sampling method). Sampling kits are obtainable from the Animal Health Trust webshop AHT DNA Testing. Further information can be obtained by emailing e-mail

Share this with:
Delicious

Beautiful and healthy

Presenting valuable show dogs at national or international Kennel Club meetings or Dog Shows is a full-time job: not only must the four-legged candidates be healthy, in top-shape and perfect form – also cosmetical aspects play an important role to win the Show and be a CHAMPION!

No Dog Show allows unhealthy dogs to be presented in the ring, and every effort must be taken to avoid any possible hazard of spreading infectious diseases between the show dogs. Effective control mechanisms, mostly under the supervision of veterinarians, are established at least in the larger and more important shows, to sort out dogs with diseases, fever or non-tolerable behaviour.
But who looks into the mouth?

Very often the judges inspect the oral cavity very meticulously, because a healthy, clean and correctly developed dentition and skull is a paramount part of the general appearance and status of any candidate. Skull, alveolar bones and dentition have to match the breed “Standard” of every registered breed. Missing or discoloured teeth, covered with slimy unhygienic masses or unpleasant odour from the mouth would not be a favourable precondition for a successful presentation.

© Roger Sjølstad UP: This 7-year old Malinois shows signs of use and wear (abrasions) but his teeth are clean, gums and periodontium are in excellent condition. © Roger Sjølstad DOWN:An “average mouth”: no signs of severe gingivitis or periodontitis are present, but unattractive discolorations and biofilms (plaque) are obvious; not good enough for a CHAMPION.

An unhealthy and unattractive dentition is in most cases caused by periodontal disease, which is the most common of all diseases in mammals. More than 80 % of all adult individuals – may that be cats, dogs or humans – suffer from it. The prevention of periodontal disease is a life-long struggle which includes home-care, appropriate nutrition and – if unavoidable – professional veterinary treatment.
As always – prevention is better than cure

Only approximately 10 % of pet dogs receive daily oral hygiene, this means that many dogs suffer from a very poor condition in their mouth, continuous active infection, associated with permanent pain, finally loss of function due to lost teeth and or even organ infection.

As a precondition for successful work with breeding dogs and show dogs, owners of these animals have a by far higher motivation (and education) and take good care of the overall health and dental condition of their precious dogs. Regular tooth brushing, appropriate nutrition, systematical controls and health checks at the veterinarians are of paramount importance. For every showdog, daily tooth-brushing with special toothbrushes and tooth-pastes is highly recommended. Never use human tooth-pastes, they are not only badly accepted by dogs, but also contain ingredients, which can damage the gums. If discolorations are detected, tartar-build up or halitosis is present, the veterinarian should be contacted.
Bad teeth – bad ranking

Not too long before important shows, the dog should be seen by a vet and – if necessary – get a complete dental check and prophylaxis , which means a thorough cleaning and removal of all soft biofilms (Plaque) and hard mineralised debris on the dental surfaces (Tartar, calculus). The teeth should be polished after cleaning to avoid rough dental surfaces after the procedures, which would allow new plaque to recolonise again very quickly, making repeated procedures necessary year after year. Dental plaque is highly pathogenic and the primary cause of both gingivitis and periodontitis or even tooth loss. In addition these aggressive plaque bacteria can enter the blood stream and be spread across the whole body, which may cause septicaemia and organ disease.

The accumulation of dental plaque on the dental surfaces is the primary cause of Gingivitis and Periodontitis, thus the key for success in preventing such periodontal conditions is control of the plaque -> no plaque – no gingivitis/periodontitis!

The benefit of professional periodontal therapy is short-lived unless followed by effective home care. Regular tooth brushing is the best method to achieve that, but both owners and dogs are not always able to handle this, also oral medications can help to reduce plaque.

The role of nutrition

Foods which encourage plaque build-up should be avoided. This includes snacks between meals, high carbohydrate foods such as table scraps, sweets and others unnatural food for dogs. Feeding specially formulated nutrition (specific dental diets, diets with an included dental benefit across the range, dental chewing sticks) is an additional effective way to reduce the amount of plaque in the oral cavity.

I recommend:

Regular professional check-ups and cleanings at your vet, once or twice a year
Daily tooth brushing and chewing toys
Feeding a diet that reduces plaque and tartar build-up

Dr.med.dent. Dr.med.vet. Peter Fahrenkrug
Dentist, Veterinarian and expert in Veterinary Dentistry

Dr. Dr. Fahrenkrug is one of the internationally leading experts in canine dentistry.

This educational article has been brought to you by EUKANUBA

In my brief five years of judging, I cannot count how many times I have communicated to exhibitors that I am not judging a statue. I offer this as relaxing encouragement to them while they attempt to correct their dog’s stance as it is being examined. However, many handlers persist, sometimes in vain, to replace dog’s feet in positions that the dog has already decided were uncomfortable. Immediately after a correction, many dogs will then go on to move their other feet. At this point, it is my policy to recommend to the exhibitor not to bother fidgeting with the dog, as I politely tell the handler I can feel everything I need to feel, regardless if the dog has moved its leg or shifted its weight. Simply, I am judging a live animal and not a statue. Some exhibitors will listen, others persist perhaps because they perceive the dog’s movement as an affront to their handling skills. For clarity, references to handler is meant to be all-embracing, for any person showing a dog.

Here on this point, I offer a suggestion to exhibitors. I typically walk my dogs into their show stack. I usually do not fidget with their feet unless they are in an exaggerated stance such as “posting.” This allows the dog to feel comfortable with the process of examination, especially the Sighthound breeds who can be more averse to a stranger’s approach and hands-on exam. Moreover, walking the dog into a stance is much more relaxing as the dog usually will land and stand over their ground in a comfortable position. Remember, the sole purpose for dog shows is not a contest as to which dog can stand still the longest, in some cases in an excessively exaggerated posture. The purpose of a dog show is to select and adjudicate over the best of the stock to perpetuate the breed. I will quickly digress here to expound on my remark about exaggerated postures. One such profile example is frequently seen in Afghan Hounds, with many of the dog’s rear feet stacked well behind the seat bones of the hindquarters. If you dropped a plumb line from the Ischial Tuberosity (rear seat bones), it is supposed to touch the front of the toes of the rear feet, however, due to exaggeration in stance or construction, that plumb line, in some cases, is far forward of the rear feet. Commonly, when stacked in such a manner and before the dog can move, he must first bring the rear legs back up under his pelvis, with some returning to a normal stance before stepping off. Other dogs, while standing naturally or even four square, are able to lead off immediately with their front leg. If such exaggerated stances were correct for the structure of that breed, then that dog would have no need to bring its rear up and under him first before he could lead off on a front leg.

Not all exhibitors are skilled and simply fussing. My biggest point of disagreement while observing some exhibitors is the clumsy effort to correct a stack by reaching over the back, grabbing the loin and pulling the dog’s hindquarters towards themselves. This action does not achieve a relaxed stance in which the judge can reflect upon and appreciate a lovely silhouette. Instead, this grappling produces a dog who was just dragged into position and who now is flexed and tense. Never mind it is very uncomfortable for observers – effectively making us cringe – and usually the handler does not stop there. After they drag the back end of the dog over to a side profile, they begin wrestling feet into place. This struggle is no more graceful than the first as the exhibitor pushes and pulls, then drags feet backwards and forward. Sometimes it is comical as the judge gives up or is impatient and approaches the dog while the exhibitor is still wrestling with the feet, head bent down with their buttocks up in the air. A solution for inexperienced exhibitors is taking five minutes every day to work with the dog by teaching it to walk forward into a stack. The stack does not have to be perfect because, again, we are not judging sculpture. Teach or train the dog on its show lead — not a walking lead so they can differentiate when they are working — and train the dog to walk slowly forward as they place their front legs straight up and down with elbows directly under their shoulder blades, their hocks perpendicular to the ground. When showing, if one leg is back somewhat, don’t fret, leave it. If the dog’s stance is still unacceptable to you, correct it after the judge has completed their exam and not while the judge is examining the dog. After the judge is finished, quickly readjust or if it is a body shift then slowly walk the dog forward one or more steps to the desirable stance. Every judge should allow the exhibitor the few extra seconds, if the handler chooses to do so, to walk the dog forward a step to correct a bad stack. This is courteous to do so since it is the exhibitors hard-earned money paying the judge for the evaluation, not visa versa. Likewise, walking into a stack is a bonus for bona-fide judges, those not looking at their wristwatch, as most dogs tend to relax and settle into themselves quickly. No matter the handler’s choice, just please stop wrestling.

Conformation purebred dog events have been transformed into a showing and grooming contest. Today we observe many firmly established handling habits. Exhibitors will place huge emphasis on a dog’s stack while on the table or ramp. If the dog moves, the exhibitor constantly makes corrections, as if the judge will not be able to feel the placement, angulation and length of the bones and muscling, or quality of coat if a foot is out of place. Moreover, exhibitors need to remember that judging does not take place on these elevated platforms, only examinations. Dogs are only judged on the ground. If the opposite were true then each of these dogs would be exhibited on a table or ramp in the ring always. Perhaps this habit has manifested itself so widely because exhibitors follow the lead of many professional handlers who have perfected the ability to emphasize perfect, statuesque stacks. Consider an exhibitors reaction the instant a dog moves their head to look around while stacked in the lineup. Many have a death grip on the muzzle. A reminder to everyone in our sport, dogs should not receive extra consideration for being able to stand still the longest.

Other established and trying habits include handlers overemphasizing certain breeds abundance of thin, loose skin, wrinkles or folds. Short-coated breeds are “what you see is what you get.” Still, we have exhibitors over-accentuating by grasping and pulling the skin up and forward. The judge is not blind and can clearly see and feel the skin’s looseness, along with scapula placement, without the aid of the handler. As an extra factor, I have heard disapproving comments by spectators. Although we seasoned fanciers understand this does not hurt the dog, no amount of reassurance can change some people’s minds. Taking into account the purebred dog controversy in place today, we can do away with such unnecessary elaboration. Another annoying and dispensable habit during examination are handler’s stretching dog’s neck, pulling upwards, almost lifting the dog’s front off the ground and then flipping the ears over both eyes — all in a grandstanding effort to feature the neck on a smooth or short-coated breed. Speaking plainly, a judge is quite capable of discerning a proper neck without all this dramatizing, especially since most are approved to judge heavy-coated and long-coated breeds. If the judge requires or encourages such elaboration on a neck then they should reevaluate their role in our sport.

Dog shows were not meant to be a contest of animal or people showmanship. Our shows were not created or designed to determine who is the more flamboyant handler, for instance the handler standing out nearly four feet in front of the dog waving a piece of bait in their free hand. Some handlers claim that the dog who is posed looking very much like a sculptured bronze is, indeed, in a natural stance. Occasionally, this may be true and usually can be determined by directing the handler to move the dog around to the center of the ring and having them stop without touching the dog. Few times will the dog land as they were previously stacked. Many times, the dog will land and stand much more naturally, which a true breed expert will appreciate moreso than an over-dramatized stance. In truth, show dogs increasingly now are trained to stop and self-stack in dramatic poses without interference by the handler. Yet, what I would find most telling is if we were to see the same dog running and playing in the yard or field they most likely stop and stand in an entirely different manner contrary to dog show pageantry.

Aficionado judges appreciate the dog without the glamour and fanfare. An enhancement to this and what I consider exciting is to find a truly well-made dog who feels good under your hand who may not be the showiest entry in the ring but who epitomizes the breed standard. To be able to “find” a great dog in the show ring is the ultimate reward. My usual response is to quietly laugh when I read judges interviews or hear their commentary on dogs they have awarded. I am sure you all are familiar with, “The dog gave it their all,”; “The dog asked for it and could not be denied,”; “The dog showed beautifully,” ; “The dog was so on,” ; “The dog has attitude.” Conversely, “The dog did not perform that well,”; “The dog could have been more on.”

Taking into account these critiques, it is no wonder almost all exhibitors fret constantly about a misplaced foot, constantly adjusting and readjusting legs, death grips on the muzzles, stretching out necks, pulling the skin over the dog’s face and so on. These dispiriting comments all highlight the non-essentials of our sport. Why place more value on the dog flying around the ring at the end of their lead, many at incorrect speeds? Why do judges value the dog in an aggrandized, statuesque stance moreso than its competitor(s) who may fidget but who stands over their ground in a comfortable, confident manner sans embellishment? Doesn’t breed type and symmetry trounce being overdone and flamboyant? We should all worry about the general direction in which our sport has developed. It is deeply concerning and saddening for many veterans. Over the years, our sport has been steered towards glorifying and worshipping the most highly trained and unflinching statues. This is a show with live animals, not a statue exhibition. Though I would not nor am I suggesting a dog should be penalized for being perfectly trained and very stylishly shown, at the same time a judge should not bestow additional merit on this dog over its competitors based upon this ability to attract, in many cases, undue attention. However, we are very much aware of this or similar preferences by some judges through their critiques. Absent from reviews are conclusions on a specimen’s structural integrity, the virtues of that dog’s priceless breed type expounding on the near flawless shape, describing the breed’s topline and underline, discussing the prosternum, its fill and relative station and length of ribbing. Going into detail about the dog’s diameter and length of bone, the breed standard’s ideal length, strength and breadth of loin or the opposite, well-coupled with strong breadth of loin, or remarks on the symmetry of the dog’s conforming length and placement of scapula/humerus in relation to the femur/tibia, or any mention of superior muscling. On occasion, we do hear vague comments about headpieces as they are first discernible and easiest to describe. All the same, the comments provide little insight such as, “What a lovely head.” We do not read instructive remarks about proper length of planes with degree of desired stop, eye set and shape, width or shape of skull and muzzle.

Overall, in place of educational particulars, we are provided nebulous, frivolous comments. This may be due in part to judges’ inexperience with formulating and expressing their opinions, remarks and reactions to the dogs. Many quality judges with a keen eye instinctively know a good or great dog when they see one and have trouble conveying why, then there are other judges who skate by with a quick but insubstantial remark about, “how spot on” a dog was in the ring. What is the value of saying this? How does that have anything to do with the breed standard for which the dog is judged? It is no wonder that our sport is filled with uninstructed, naïve exhibitors and breeders. If they hear or read a judge’s explanations about the winning dogs and all they are offered are the aforementioned, meaningless comments, then it should come as no surprise that our sport has devalued. These comments undermine the importance of, the genuine purpose of our sport, why and how it began. It does not have to be this way. We judges can effect change, have a marked influence on breeder and exhibitor priorities which, in turn, will return focus on breeds’ standards of excellence. As I am very fond of repeating, we need to get back to the basics.

]]> http://newacdgazette.com/2013/01/07/we-are-not-judging-statues/feed/ 0 61.677774 23.450500 61.677774 23.450500 acdisla fox http://newacdgazette.com/2012/12/22/coat-colors-of-the-australian-cattledog/ http://newacdgazette.com/2012/12/22/coat-colors-of-the-australian-cattledog/#comments Sat, 22 Dec 2012 03:13:55 +0000 acdisla http://newacdgazette.com/?p=8521 Continue reading →]]>

AND AUSTRALIAN STUMPY TAIL CATTLEDOG Standard Colors Black ticked called “BLUE” and sable-ticked called “RED” Non-Standard Colors YELLOW E/E BROWN WHITE As more research is conducted in the field of (color) genetics, more information gathered and more of the ‘unknowns’ are ‘known’ — this website will be updated to reflect that information. Definitions: chromosome: The nuclear structure which houses (contains) the genetic information. Chromosomes exist in pairs and therefore there are always two copies of a given gene. gene: a unit of inheritance locus (-ci): the position of a gene on a chromosome. Every gene has a specific locus genotype: the genetic make-up of an individual phenotype: that part of the physical appearance of an organism which depends on gene action homozygous: the condition when both alleles of a gene pair are identical heterozygous: the condition when both alleles of a gene pair are different dominant: term describing a gene which can produce a phenotype when present only once; also the phenotype which results recessive: term describing a gene which must be present twice to produce a phenotype; also refers to the phenotype which results wild: the “normal” phenotype mutant: the non-normal phenotype; is a relative term (relative to the population from which the organism originates color genes: genes that affect the pigment color of hairs pattern genes: genes that affect the distribution of a particular color. Different terms are sometimes used for the same genetic colors, depending on breed and sometimes country too. In Dobermans, the dilute brown, is called Isabella. In Border Collies, the dilute brown, is called Lilac. In Kelpies, the dilute brown, is called Fawn. A dog that is genetically ‘recessive red’ (“e/e”) is known as yellow in some breeds and red in others. Brown is called chocolate by many and is also referred to as red. In the ACD breed, the ticked- black/tan is known as blue and the ticked-sable is called red. This is confusing at times. MELANIN, AGOUTI AND RED: Melanin is the substance that gives a dog’s hair its color. There are two distinct types of melanin in the dog — eumelanin and phaeomelanin. Eumelanin is, in the absence of other modifying genes, black or dark brown. Phaeomelanin is, in its unmodified form, a yellowish color. Melanin is produced by cells called melanocytes. These are found in the skin, hair bulbs (from which the hairs grow) and other places. Melanocytes within the hair follicles cause melanin to be added to the hair as it grows. However, melanin is not added at a constant ‘rate’. At the very tip of the hair, eumelanin production is usually most intense, resulting in the darker tip. A protein called the Agouti protein has a major effect on the amount of melanin injected into the growing hair. The Agouti protein causes a banding effect on the hair: it causes a fairly sudden change from the production of eumelanin (black/brown pigment) to phaeomelanin (red/yellow pigment). An example of this coloration would be like the color of a wild rabbit. The term ‘Agouti’ actually refers to a South American rodent that exemplifies this type of hair. The Extension Locus – E This refers to the extension of eumelanin over the dog’s body. The dominant form, “E”, is normal extension. The recessive form, “e”, is non-extension. When a dog is homozygous for non-extension (e/e), its coat will be entirely red/yellow (phaeomelanin based). All dogs that have a brown (chocolate) coat will have at least one “E” allele, because of the production of eumelanin. The way to tell the difference between an Agouti red/yellow and an Extension (e/e) red/yellow dog — is the Agouti red/yellow almost always have some black/brown hair in the coat (usually around the ears and tail) and the Extension (e/e) dog won’t. Another way is the Agouti red/yellow must have at least one (“A^y”) allele and can carry at most one other agouti allele, the Extension (e/e) can carry any two Agouti alleles (not necessarily “A^y”). DOMINANT BLACK — “K” The dominant form of black: completely dominates all formation of phaeomelanin pigment. In the past, dominant black had been placed at the head of the Agouti series (symbol “A^s”). Now, it has been proven to be part of a separate series, the “K” series, and not at the Agouti locus at all. Dominant black (K) is epistatic to whatever is found at the Agouti locus (simply means that it causes the Agouti allele to act differently from what it normally would), however; “e/e” is dominant to “K” at the E locus. When “K” is in the dominant form, “K/K” or “K/k”, there would be no expression from the A Locus and the color is dependant on what is at the E Locus. When “K” is in the homozygous recessive form “k/k”, the coat color will depend on what is located on the “E” and “A” Locus. Dominant “K” codes for both dominant black and brindle in decreasing order of dominance: K — dominant black (does not allow the A Locus alleles to be expressed) k^br — brindle (expressed when A Locus alleles are expressed) k — normal (allows the A Locus alleles to be expressed) A dog that is: K/K or K/k — dominant black; dominant black carrying recessive black k^br/k^br — brindled k^br/k — brindled, carrying recessive black k/k — ‘normal’ (recessive black) Brindling is ‘stripes’ of eumelanin-based (can be modified by the genes at the B and D Locus, so the color could be black, blue, chocolate or fawn) hairs in areas that are otherwise phaeomelanin based. In order to produce the brindle color, at least one parent MUST be a brindle. Brindle is dominant to its absence, so only one copy is needed. If a person has a brindle colored pup for sale and there are no brindle colors anywhere in the pedigree, then the sire that is reported on the registration papers — genetically can not be the (true) sire. There is an exception to this if the dog is “e/e”, he can be a carrier of brindle. It is thought that the three loci E, K and A act together as follows: If the dog is “e/e” at the E locus, and at the K locus, it is “K”, “k^br” or “k”, its coat will be entirely red/yellow (phaeomelanin based); If the dog is E/E or E/e at the E locus, and at the K locus, it is “K/K” or “K/k”, its coat will be entirely dominant black (eumelanin based) [**NOTE: the phenotypic color will depend on what is at the B, D, C and M Locus]; If the dog is E/E or E/e at the E locus, and at the K locus, it is “k^br/k^br” or “k^br/k” it will be brindled with the color of the phaeomelanin part of the brindling affected by the Agouti alleles present; If the dog is E/E or E/e at the E locus, and at the K locus, it is “k/k” the distribution of eumelanin and phaeomelanin will be determined solely by the Agouti alleles present. The Agouti Locus – A Simply, this is how the pigment is distributed on the dog’s body and hair shaft. The Agouti locus controls the formation of the Agouti protein, that in turn is one of the mechanisms that controls the replacement of eumelanin with phaeomelanin in the growing hair. The alleles of the Agouti locus can affect not just whether or not the eumelanin — phaeomelanin shift occurs, but also where on the dog’s body this happens. Two promoters are generally associated with the “wild type” version of the agouti gene. Cycling Promoter Ventral Promoter The Cycling Promoter produces a banded hair with a black tip and yellow middle over the entire body. If only the action of this promoter is disrupted, the hair color on the dog’s back will be black and its belly and inside of the legs will be yellow. This produces the black and tan color. The Ventral Promoter dictates that there will be only yellow color in the hair on the belly. The animal will have black banded hair on the dorsal (back) side and paler yellow hair on the ventral (belly) side. If only the action of this promoter is disrupted, the hair color on the dog will be banded over its entire body. This is said to be solid agouti color. If something inactivates the agouti protein, or if both promoters are disrupted, the animal will appear to be solid black. If a mutation occurs at one of these Promoters, this can cause the yellow to be expressed over most of the body. NOTE: In part of a series on Dog Coat Color Genetics by Sheila Schmutz, she states that recent studies show that the agouti signal peptide (ASIP) competes with melanocyte stimulating hormone (MSH), which produces eumelanin pigments, to bind on the melanocortin receptor and must sometimes win. Both the E allele and Em allele are responsive to agouti or melanocortin binding in dogs. However dogs that are ee have a mutation in MC1R and produce only phaeomelanin. The dog’s agouti genotype doesn’t affect its coat color, which will be some shade of cream, yellow or red. To further complicate things, agouti has 2 separate and somewhat distant promoters. Roughly, one seems to control ventral or belly color and the other dorsal or back color. The simplest way to “see” this is on a black and tan dog……the back is black from eumelanin pigment being made and the belly is tan or red from phaeomelanin pigment being made. The agouti gene has been mapped in the dog and DNA studies to determine which patterns are under the control of this gene in the dog are in progress. This gene undoubtedly has several alleles, but how many is still an open question. Some have been identified using DNA studies and tests for agouti phenotypes in some breeds may become available soon. Although several books attempt to state the dominance hierarchy of the agouti alleles, since no breed has all the alleles, it is not possible to know this for sure. Most books suggest that it is aw > ay > at > a. Breeding data and DNA data from our collaborative study with Dr. Greg Barsh’s group at Stanford supports this. However the data confirm pairwise dominance/recessive relationships in different families…….not the entire hierarchy in one family. Decreasing in order of dominance: (**sable may be dominant over wolf in some breeders) “a^w”, ‘wolf’ color – This is like “a^y” but the tan is replaced with a pale gray/cream color and the hairs usually have several bands of light and dark color, not just the black tip of sable. Example would be Keeshond, Siberian and Norwegian Elkhound. “a^y”, ‘sable’ – also known as ‘dominant yellow’ or ‘golden sable’. This results in an essentially red/yellow phenotype, but the hair tips are black (eumelanin). The extent of the eumelanin tip varies considerably from lighter sables (where just the ear tips are black, called “Clear Sables”) to darker sables (where much of the body is dark, called “Shaded Sables”). “a^s”, ‘saddle’ – Eumelanin is restricted to the back and side regions, somewhat like the black/tan (“a^t”) allele (below). “a^t”, ‘tan points’ – This is primarily a solid colored dog with tan (phaeomelanin) “points” above the eyes, muzzle, chest, stomach and lower legs. The hue can range from a pale biscuit to a rich ginger to a golden copper in color. Commonly seen in many breeds like hounds, Dobermans, Rottweilers and Kelpies. In breeds that have the Irish spotting, along with tan points, this is known as “tri” colored (Australian Shepherds and Border Collies). “a” – last of the Agouti series is recessive black. When a dog is homozygous for recessive black (a/a), there will be no red/yellow (phaeomelanin) in its coat (unless “e/e” is present, which is epistatic to the Agouti series). Examples of breeds that show to be recessive black are German Shepherd and Shetland Sheepdog. BLACK or BROWN (CHOCOLATE) – B GENE LOCUS: (pigment color) This gene, when in the homozygous recessive form, has a lightening effect on eumelanin (black-based colors) only. It has no effect on phaeomelanin (red-based colors). B/B or B/b – black b/b – brown It is believed that the Brown Locus codes for an enzyme, tyrosinase-related protein 1 (TYRP1), which catalyzes the final step in eumelanin production, changing the final intermediate brown pigment (dihydroxyindole) to black pigment. SO, ALL dogs start as BROWN and after the final step — this directs the color to be black. When brown (b/b) is expressed, it means that the final step in eumelanin production has not been completed and the pigment remains brown. The brown color is not a genetic defect. When the alleles are in the homozygous or heterozygous dominant form of B/B or B/b, the color and pigment (nose, eye rims and lips) remains (or directs the color to be) black. When the alleles are in the homozygous recessive form (b/b), the color and pigment will be brown. This just means that the final step in eumelanin production of changing brown to black did not occur. Phaemelanin (yellow/red [e/e]) is not affected. BUT, in the e/e colored dog, if the dog is also b/b; they will be either red or yellow and will have brown pigment (nose, eye rims and lips). The pigment granules produced by “bb” are smaller, rounder in shape, and appear lighter than pigment granules in “B” dogs. The iris of the eye is also lightened. DILUTION – D GENE LOCUS: (dilution of pigment) Not found (has been bred out) in the ACD or ASTCD breed. This gene has an effect on both eumelanin and phaeomelanin. D/D or D/d – it allows for full color (black or chocolate). d/d – homozygous recessive form dilutes black (eumelanin) to blue, red to cream, and chocolate to a dull flat color (some call it milk chocolate color). COMBINATIONS OF B AND D IN EUMELANISTIC COATS: The effects of these 2 genes, when combined, form a range of 4 eumelanistic (‘black-based’) colors: The color of the pup/dog (Eumelanistic Color): B/B D/D or B/b D/d will be black in color B/B d/d or B/b d/d will be blue in color b/b D/D or b/b D/d will be brown/Chocolate (called red in Kelpies) b/b d/d will be flat or dull diluted brown/chocolate (called fawn in Kelpies). WHITE SPOTTING – S GENE: The “S” series alleles appear to be incompletely dominant. In dogs it is thought there are four alleles that deal with white spotting: “S” – ‘solid/self color’. Most dogs that are homozygous for “S/S” have no white hair at all, or possible a tiny amount, like a white tail tip. “s^i” – ‘irish spotting’. This involves white spotting on most parts of the coat, but not crossing the back beyond the withers. This color pattern is evident on the Border Collie, Australian Shepherd and other breeds that have the white collar. New research has proven that the white undersides of the Border Collie is dictated by a different gene. “s^p” – ‘piebald’. The white is more extensive than irish spotting, and often crosses the back. It is sometimes confused with the merle pattern. This coloration usually has large colored spots on the body. The white covers approximately 50% of the body. “s^w” – ‘extreme white piebald’. A dog that is homozygous for “s^w” will be almost entirely white, like some Bull Terriers. The Australian Cattle Dog, the coloration that is called “Blue”, and “Red” by the ACD and ASTCD breeders/owners, is really the extreme piebald pattern that is also affected by the ticking gene; giving the coloration a blue appearance. This allelic pair is also responsible for the “color headed” white dogs. Often times, along with a colored head, there will also be a colored spot near the tail (called the caudle spot). TICKED – T GENE: A dominant mutation that causes the presence of color (flecks of color) in areas that have been made white by the effect of alleles in the white spotting (S) series. T/T – ticked (incompletely dominant to non-ticked). This gene is what gives the ACD and ASTCD their unique coloration. t/t – non-ticked ALBINO – C GENE: (development of pigment) The intensity of melanin production in the coat hairs is affected by this gene. The dominant form, “C”, is termed ‘full color’. At this locus, almost all dogs are “C/C”, or full color. The lower series alleles, in order of decreasing dominance: “c^ch” – Chinchilla — It is an incomplete dominant gene. Chinchilla lightens most or all of the red/yellow (phaeomelanin) with little or no effect on black/brown (eumelanin). It turns black/tan to black/silver. In dogs, this gene lightens yellow, tan or reddish phaeomelanin to cream. Since there is little effect on the dark eumelanin, phaeomelanin is effected more strongly than eumelanin and brown. Dilute eumelanin (blue) is effected more strongly than dark (black) eumelanin. When chinchilla is present, it dilutes brown to milk chocolate, blue to silver and red to a butter cream color. NOTE: Newer research indicates a chinchilla-like mutation occurs in dogs, although, tyrosinase activity hasn’t been shown to be connected. Therefore, some other factor may be involved and the dog chinchilla allele may not belong in this series. Also, there may be more than one form of the chinchilla gene. “c^e” – is ‘extreme dilution’. It causes tan to become almost white. It is thought that the white labrador might be “c^e” with another, lower, “C” series allele. The “c^e” allele may be responsible for producing white hair, while allowing full expression of dark nose and eye pigment. West Highland Terriers are thought to be e/e c^e/c^e. “c^b” – or blue-eyed albino. This is an entirely white coat with a very small amount of residual pigment in the eyes, giving pale blue eyes. It is also called platinum or silver. This allelic pair could be responsible for the white coated, pink skinned, blue-eyed Doberman’s. “c^c” – true pink-eyed albino. Has not been seen in dogs. GRAYING – G GENE: This is a dominant mutant gene that causes the dog to gray with age. The pigmented hairs are progressively replaced with unpigmented hairs. MERLE – M GENE: (ACD and ASTCD do not have the merle pattern) The only way a merle colored pup can be produced is if at least one parent is merle. Some breeders are of the understanding that the merle gene is a recessive gene and is carried from generation to generation. This is not correct. The merle gene is not carried, meaning — the dog is either a merle or is not a merle. There are no exceptions to this law of genetics (for now, at least, until further research is conducted). If someone tells you that they have a litter of merled colored pups and there are no merles for many generations in their bloodlines — then these merled pups were not sired by the sire the owner thinks there were. In fact, he should look for the hole in the fence! The merle gene is an incomplete dominant or a gene with intermediate expression and is another dilution gene. Instead of diluting the whole coat it causes a patchy dilution, with a black coat becoming gray patched with black. Brown becomes dilute brown patched with chocolate, sienna, brick, and various diluted brown colors. While sable merles can be distinguished from sables, this is sometimes very difficult because the merle coloration looks like – to just slightly different from — the sable color. The merling is clearly visible at birth, but may fade to little more than mottling of the ear tips as an adult. Merling on the tan points of a merle black and tan is not immediately obvious, either, though it does show if the mask factor is present. Eyes of a merle dog are sometimes blue or marbled (brown and blue segments in the eye). A “m/m” (homozygous recessive) dog is normal color (no merling). A “M/m” (heterozygous) dog is a merle. A “M/M” (homozygous dominant) dog, known as a double merle (from a merle to merle mating), has much more white than is normal for the breed and may have hearing loss, vision problems including small or missing eyes, and possible infertility. The health effects seem worse if a gene for white markings is also present. In Border Collies and Australian Shepherds, all of which normally have fairly extensive white markings, the “M/M” white has a strong probability of being deaf or blind. A “M/M”, double merle, to “mm”, non-merle black in color breeding, is the only one that will produce 100% merles. Cryptic or phantom (as it’s sometimes called) merles are dogs which carry a merle gene but are phenotypically (look like) tri, bi or self colored. These dogs will have some small area of merling somewhere, usually a tiny patch of merle pattern on their ear, tail, top of head, etc. Keep in mind the tiny patch can be only one hair and it can be located anywhere on the body. Cryptic merles are very rare. AGAIN, a cryptic or visible merle can only be produced when one or both parents are merles. GENOTYPES AND COLORS: (“-” is either the dominant or recessive allele) B/- D/- E/- K/- = black b/b D/- E/- K/- = brown (chocolate) B/- d/d E/- K/- = blue b/b d/d E/- K/- = fawn AGOUTI: at^at B/- D/- E/- k/k = black with tan points at^at b/b D/- E/- k/k = chocolate with tan points at^at B/- d/d E/- k/k = blue with dilute tan points at^at b/b d/d E/- k/k = fawn with dilute tan points NON-EXTENSION RED (cream): B/B d/d e/e = dilute red to pale cream with gray nose (dog is genetically a dilute black, but will be a cream color) B/b d/d e/e = dilute red to pale cream with gray nose (dog is genetically a dilute black, but will be a cream color) b/b d/d e/e = dilute red to pale cream with rosey-brown nose (dog is genetically dilute brown, but will be cream color) b/b D/d e/e = dilute red to pale cream with brown nose (dog is genetically brown, but will be cream color) b/b D/D e/e = dilute red to pale cream with brown nose (dog is genetically brown, but will be cream color) B/B D/D e/e = dilute red to pale cream with black nose (dog is genetically black, but will be cream color) B/b D/d e/e = dilute red to pale cream with black nose (dog is genetically black, but will be cream color) MORE SIMPLY: Dogs are either black or red —- other alleles act upon each other to create different colors or different shades of colors. It is theorized that all breeds of dogs have all of the alleles for different colors. Some dogs are been selectively bred over the many years to be dominant for a certain color or colors. A few examples would be the Golden Retriever, Irish Setter, Weimaraner, Lab etc… When you are looking at coat color, it is best to look at the entire picture. The entire picture being all the alleles that encode for color. We will look at each individual allele and then, later, put them together for the complete coat color. Keeping in mind that each puppy receives a copy of each allele from their parents. The first listed allele is expressed, the second one is hidden or carried. If one parent is brown (b/b) – the “b” allele is the ONLY one that can be copied and inherited by the puppy. So, the puppy will receive a copy of the “b” allele from that parent. If the other parent is B/B – the only allele that the puppy can receive is “B”. All of the offspring are B/b, or black and carrying brown. If one parent is B/b – the puppy can receive either “B” or “b”. If the other parent is also B/b – the puppy can receive either “B” or “b” (from that parent). The offspring will be: B/B – black; B/b – black and carrying brown; or b/b – brown. Genes that are carried can remain hidden for many generations. Some are under the impression that the hidden genes can be bred out in three generations, this is always not the case. Pigment distribution patterns are controlled by the A and E Loci. Color that is modified by diluting colors are controlled by the B, C, D, G and M Loci. The placement of white areas on the coat are controlled by the S and T Loci. K Locus: controls the expression of the A Locus and brindle K/K or K/k – does not allow the expression of the A Locus (the alleles are still present, just not allowed to the expressed) or brindle (all ticked/black ASTCD’s and ACD’s are either K/K or K/k) k^br – encodes for brindle (in order for brindle to be expressed, the dog MUST be able to express the alleles from the A Locus) (ASTCD’s nor ACD’s carry the gene for brindle) k/k – allows expression of the A Locus alleles (all red [sable] ASTCD’s and red [sable] ACD’s) E extension: controls the extent of black (eumelanin) or yellow (phaeomelanin) across the coat. E/E or E/e – black coat (keep in mind we are only talking about one allele, when other alleles are added, the color could change) e/e – red or yellow coat (this is a mutation and does not allow black to be expressed. It is epistatic (means causes other alleles to act differently from what they normally would) to all other alleles, but can be modified by the C Locus to be lighter *NOTE: Red (e/e) has been found in the ASTCD and ACD A Locus: Controls the amount of black and yellow color placement on individual hairs. a^y – Sable: red shaft with black tips (genotype of the red ASTCD and red ACD) a^w – Wolf: banded coloration; eumelanin and phaeomelanin compete with each and this causes the banding of color – light, dark, light, dark (not found in the ASTCD nor the ACD) a^s – Saddle: no one is sure if this is a separate allele from tan points, or just an exaggerated pattern (can be a carried allele, although not regularly found in the ASTCD, has been seen in the ACD) a^t – Tan points: eumelanin covering most of the dorsal (back) surface with phaemelanin on the legs, throat, chest, above the eyes, cheeks and underneath the tail (genotype of the ACD and found in some ASTCD; can be a carried allele) a^a – recessive black: Only a few breeds are recessive black, usually found in herding breeds (Australian Shepherd, German Shepherd) and the Schipperke (studies are now being conducted concerning the inheritance and location of this gene) *** NOTE: there are two promoters that are associated with the A Locus. The cycling promoter produces a banded hair with a black tip and yellow middle over the entire body. The other is the ventral promoter that directs there be only yellow color in the hair on the belly. These work together and the animal will have black banded hair on the dorsal surface and paler yellow hair on the ventral (stomach) surface. B Locus: Controls ONLY eumelanin (black) to either a modification of or full color. Also controls skin pigment (eye rims, lips and nose leather) and iris color. It is believed that the Brown Locus codes for an enzyme, tyrosinase-related protein 1 (TYRP1), which catalyzes the final step in eumelanin production, changing the final intermediate brown pigment (dihydroxyindole) to black pigment. SO, ALL dogs start as BROWN and after the final step — this directs the color to be black. When brown (b/b) is expressed, it means that the final step in eumelanin production has not been completed and the pigment remains brown. The brown color is not a genetic defect. When the alleles are in the homozygous or heterozygous dominant form of B/B or B/b, the color and pigment (nose, eye rims and lips) remains (or directs the color to be) black. When the alleles are in the homozygous recessive form (b/b), the color and pigment will be brown. This just means that the final step in eumelanin production of changing brown to black did not occur. Phaemelanin (yellow/red [e/e]) is not affected. BUT, in the e/e colored dog, if the dog is also b/b; they will be either red or yellow and will have brown pigment (nose, eye rims and lips). The pigment granules produced by “bb” are smaller, rounder in shape, and appear lighter than pigment granules in “B” dogs. The iris of the eye is also lightened. B/B or B/b – is full color, does not change skin pigment or iris color b/b – the last step in the production of eumelanin is missing, therefore; the color is brown (not red). This allelic pair does change skin pigment and iris color (no matter what other alleles are present). (This coloration has been found in the ASTCD and the ACD). ***NOTE: there are actually 3 different alleles that encode for the brown color, since they all do the same thing, only one is mentioned.D Locus: Controls BOTH eumelanin and phaeomelanin to either full color or dilution. Also control skin pigment (eye rims, lips, and nose leather) and iris color. D/D or D/d – controls full color (black or red) (ASTCD’s and ACD’s are thought to be homozygous for this allele [D/D]) D/D or D/d – no dilution, codes for full color d/d – dilutes any other alleles present (example: dilutes e/e to pale yellow; dilutes b/b to a flat silvery-brown dull color; dilutes sable to yellow), also dilutes skin pigment of the eye rims, lips and nose leather to gray and lightens the iris color. C Locus: Controls full color or dilutes the color C/C – full color, no dilution (keep in mind the b/b and d/d will dilute the alleles regardless) c^ch – chinchilla gene: is incompletely dominant and is a flat color. Is said to not greatly affect black and has little effect on solid black dogs. It affects lighter hues more so than darker, therefore; it lightens yellow, tan and red hues to cream, brown becomes milk chocolate or a lighter brown and blue becomes silver. c^e – extreme dilution of color. Dilutes red and yellow color to a silvery color approaching white. West Highland Terriers are thought to be “e/e c^e/c^e”. c^b – blue-eye albino. Very rare. May be responsible for the blue-eyed, pink skinned, white Doberman. c^c – true albino. Pink eyes. Not seen (yet) in dogs. S Locus: Controls white areas on the body S/S – Self colored, no white areas are expressed. Sometimes a very minimal amount of white can be found, like a white tip on the tail, white toes, white star on chest – these white areas are also thought to be caused by another allele. s^i – Irish spotting: white collar, white on legs, white on tail. White does not cross between the withers (shoulders) and tail. s^p – Piebald: white covers 50% of the body and will cross between the withers and tail. There are well defined colored spots on the body (like some Jack Russell’s). (ASTCD’s and ACD’s that have body spots are piebald). s^w – extreme piebald: white body with colored heads and usually a spot near the tail. Some dogs may have color only around the eyes or ears (or both). Breeding extreme white dogs may result in all white offspring. (All ASTCD’s and ACD’s are the extreme piebald coloration, along with being ticked [the ticking gene]). T Locus: Control small spotting on the body T/T – ticking: can only occur in areas of white color. The T and S Locus compliment each other; in other words – white areas must be present in order for the ticking to be expressed. The color of the tick (small spotting) is the color that the coat would have been, if the white spotting gene was not present. (All ASTCD’s and ACD’s have this gene). T/T or T/t – ticked or roan t/t – non-ticked G Locus: Graying gene G/G or G/g – animal grays with age, like a human g/g – does not gray M Locus: Controls the dilution of a dogs coat in a patchy pattern (incomplete dominance). Both normal color and diluted colors occur, because the M alleles are incomplete dominant. M/M – double merle; occurs when merle is bred to merle M/m – merle; occurs when merle is bred to non-merle m/m – non-merle (ALL ASTCD’s and ACD’s are non-merle)

]]> http://newacdgazette.com/2012/12/22/coat-colors-of-the-australian-cattledog/feed/ 0 0.000000 0.000000 0.000000 0.000000 acdisla lunasred218 islanelja218 http://newacdgazette.com/2012/10/08/one-year-old-cece-herding/ http://newacdgazette.com/2012/10/08/one-year-old-cece-herding/#comments Mon, 08 Oct 2012 15:26:47 +0000 acdisla http://newacdgazette.com/?p=8478 ]]> See Gwen’s young ACD herding big cattle. She has matured into a wonderful working cattle dog, terrific positive and happy temperament and eager to learn and please