Bengal Cat Genetics

Traditionally the various coat color and effects are described in alphabetical order by Locus (location) but I find this order more helpful as it builds from the skin up.

 

 

B Locus: Primary Color

Black = B - Dominant - if a cat receives this gene from one of it's parents, the cat's primary color is black.
Chocolate = b - Recessive to B
Cinnamon = bl - Recessive to B, b

Most Bengals have black as their primary color. The colors Chocolate and Cinnamon are recessive colors that exist in the breed. A cat can carry Chocolate or Cinnamon and not exhibit the color so it is important to know a breeding cats genetics. If two cats are bred that carry for Chocolate, there is a chance of the kittens being Chocolate. If two cats are bred that carry for Cinnamon, there is a chance of the kittens being Cinnamon. Chocolate and Cinnamon are not recognized colors in some registration organizations and cannot be shown there. For a cat to be chocolate or cinnamon he or she must receive the gene from both parents. For the colors Blue, Lilac and Fawn please see the D Locus.

Chocolate, b, is recessive to black. Chocolate is not recognized in most registries of the Bengal cat. Cinnamon, bl, is recessive to both black and chocolate. The pawpads and the tail tips are Chocolate and Cinnamon. This is one of the main ways to identify that a cat is not a brown/black tabby.

C Locus: Color Exhibition (The Full Color Locus)

C = Full Color - Dominant
cs = Colorpoint Siamese (the gene that causes Seal Lynx Point) - Recessive to C
cb = Colorpoint Burmese (the gene that causes Seal Sepia) - Recessive to C, incompletely dominant to cs
ca = Blue eyed Albino - Recessive to C, cs, and cb
c = Pink eyed Albino - Recessive to C, cs, and cb

You will note that there is no gene listed for Seal Mink. Seal Mink is caused by the combination of cs and cb genes. A Seal Mink receives Seal Lynx Point from one parent and Seal Sepia from the other. Just like other recessives a cat can carry the genes and not display them. Bengals carrying for "snow" are quite common and surprise white kittens can show up from two brown marbled or brown spotted cats. Both cs and cb are an albino variant found in the Siamese and Burmese breeds. True albino come in two forms, blue eyed and pink eyed. An albino Bengal will not display a pattern even if it has the Agouti gene. Albino cats often have a number of health related issues including vision problems, skin problems, and sensitivity to light.

A Locus: Agouti Banding

Agouti = A - Dominant - Pattern Displays
Non Agouti = a - Recessive - Pattern Does Not Display

This is the gene that determines if the tabby pattern will display or not. All Spotted or Marbled Bengals are Agouti/A - the pattern displays. However an all black Bengal, a Melanistic, is Non Agouti - the pattern does not display and the primary color, Black, is seen everywhere. Non-agouti is recessive and a cat must receive the gene from both parents for the pattern to be prevented from displaying. The gene can hide for several generations in a line.

Mc Locus: Pattern Flow

Mackerel Tabby = Mc - Vertical Flow
Classic Tabby = mc - Circular Flow

A Mackerel Tabby pattern means the flow of the cats pattern is more vertical, up and down. This is where the vertical barring can come from. The Classic Tabby pattern means the flow of the pattern is circular on the body of the cat. Many Bengals have the pattern flowing in a circular manner on their sides. But where does the Horizontal Flow we see in the Asian Leopard Cat and many champion bengals come from. There are two theories:

1.) The gene combination Mcmc creates Horizontal Flow. The problem with that theory is you don't see Horizontal Flow in any other breeds that don't use some form of leopard cat for their foundation

2.) A new theory is that there is another gene being labeled mz that comes from the Asian Leopard Cat, and it is found on the same Locus. If this theory is true it may be the gene that makes the Horizontal Flow we strive for, and mzmz may be what makes some of the cutting edge cats so great.

Sp Locus: Pattern Interruption

Interrupted Pattern = Sp - Dominant - The pattern is interrupted producing "spots"
Uninterupted Pattern = sp - Recessive - The pattern is continuous creating a "marbled" effect

This is where our spots and marbles come from. Little is know about the genetics that make the differences in the spots at this time. Clearly there is a genetic piece causing round spots, arrowhead spots, two color rosettes, two color arrowhead rosettes and paw print rosettes. It is hoped that this genetic database will help us get to the point where we can develop provable theories behind the genetics.

T Locus: Ticking Locus

Ticked = T - Dominant - Agouti Band covers all but the base of the shaft
Not Ticked = Ta - Recessive - Agouti band pushed off the shaft of the hair

Ticking contributes to the intensity and contrast of the pattern by determining how much of the shaft is the base color (Black, Chocolate or Cinnamon). A highly Ticked cat will only have a narrow Agouti yellow band at the base of the shaft in the pattern. While T is dominant not receiving the gene from both parents does reduce the intensity indicating that the dominance may be incomplete. A cat that is TaTa will not show the Agouti pattern because the primary color is pushed off the shaft (like an Abyssinian).

Wide Band Locus: Agouti Banding Variable

Wide Band = Wb - Dominant
Not Wide Band = wb - Recessive

Wb means that the agouti banding is made wider, thus more uniform and not as "ticked" looking. It is not known if this is a gene perse or a group of polygenes at this time. The wide band polygene affects the Agouti portions of the shaft where the emelanin (black) is turned off making them wider, sometimes so wide that the additional affects of the Agouti banding are pushed off the shaft giving the shaft a single color. It may be the source of the "clear coats" we see in the Bengal Breed.

I Locus: Inhibitor (also called the Silver gene)

Color Inhibited = I - Dominant (incompletely dominant to i)
Color Not Inhibited = i - Recessive

This gene affects the display of the yellow pigment on the Agouti banding by suppressing it. Working in tandem with the Agouti gene suppressing the production of phaeomelanin pigment (yellow/red), it has little or no effect on the emelanin pigment (black) production. With no production of phaeomelanin the shaft is left only with whatever emelanin production is occuring. If there isn't any, the shaft is white, if there are trace amounts the shaft is gray. The end result is that the shaft of the hair will look gray or white while tipped with the primary color (preferably black). This gene is dominant and only one parent needs to carry the gene for it to express. This is a very difficult gene to work with however and the color inhibition may be incomplete. In some cases break though of the phaeomelanin (yellow/red) occurs (Robinson's 142). This seems to only happen in silver cats that have one Inhibitor gene from one parent, and a Non-inhibitor gene from the other parent. This suggests that perhaps while the Inhibitor gene is dominat it may be incompletely dominant, or that there is a limit to the amount of phaeomelanin (yellow/red) it can supress when not homozygous.The resul is that by allowing the yellow to brown pigment to display the cat has what is called tarnish. Tarnish is very undesireable.

D Locus: Color Density

Dense Color = D - Dominant
Diluted Color = d - Recessive

This gene affects how the color cells in the shaft of the hair are dispersed. Normally the color cells are evenly distributed along the shaft of the hair, this is Dense Color and it is what we see in most Bengals. However if the color cells in the shaft of hair clump together they don't demonstrate the full coloring of the primary color making the shaft look "frosted" properly called Dilute. To be dilute the cat must receive the recessive d from both parents as dd ... DD and Dd will not show the diluted or frosted appearance. This is where the Bengal colors Blue, Lilac and Fawn come from. Blue is actually diluted Black, Lilac is actually diluted Chocolate, and Fawn is actually diluted Cinnamon.

O Locus: Orange

O = Orange
o = Not Orange

Orange is the elimination of all eumelanistic (Black) pigment by converting the proteins into phaeomelanin (yellow). It comes from the Torbie influence used as an early outcross in the Bengal breed. This is not to be confused with rufousing. It is sex linked carried on the X chromosome so only females may exhibit it. The Orange gene is not common but it has surfaced in the breed from time to time.

Mi Locus: Mica Glitter

Non-glittered = Mi - Dominant
Glittered = mi - Recessive

This gene is still partially theory. It affects just the tips of the hair shaft. In the recessive form, mi, when we look at the hair shaft under a powerful microscope we see what appear to be small flecks of Mica, a very reflective mineral, embedded in the tip of the hair shaft. We hope to post pictures of this effect on this page in the future. This gene did not come from the Asian Leopard Cat but rather from a domestic cat used by Jean Mill in her early breeding program. Another form of glitter runs the full length of the shaft, please see the Sa Locus for more information on that glitter type.

Sa Locus: Satin Glitter

Sa = Non-Satin - Dominant
sa = Satin - Recessive

This gene is still very much in the theory phase. This gene is seen in several species. Inter species genetic comparison is common. Many mammals are genetically similar and traits found in one species may also crop up in another.

The satin gene is well documented in some rodent species including mice and rabbits. It is also believed to be in Bengals coming from some of the domestic cats that were used as outcrosses in the Bengal such as Siamese, Burmese, Ocicat and Egyptian Mau. This gene creates little bubbles of air in a sheath that surrounds the full length of the follicle. These air bubbles catch and refract the light giving the coat a glittered effect which, while similar in some respects to the Mica Glitter, it is also very different. This gene also makes the shaft of the hair very smooth and gives the cats coat a very soft and silky feel. The more satin shafts in the coat the silkier and softer the fur.

L Locus: Hair Length

L = Short Hair- Dominant
l = Long Hair- Recessive

The long hair gene doesn't crop up very often in the Bengal breed, but it is out there. Bengals are intended to be short hair but the occasional long hair kitten crops up. They are gorgeous and loving and make a great friend. They are not currently showable and are usually only available as pets.

 

 

 

I will be updating more on this page as information comes to me.

 

 

 

 

HYPERTROPHIC CARDIOMYOPATHY

Etiology

The cause of primary or idiopathic hypertrophic cardiomyopathy (HCM) in cats is unknown, although a genetic basis or predisposition is likely in some cases. The disease appears to be highly prevalent in certain bloodlines of several breeds. Most cases of HCM in people are familial, and several specific abnormalities of genes for myocardial proteins have been identified in different kindreds. In addition to mutations of genes that encode for myocardial contractile or regulatory proteins, postulated causes of the disease include an increased myocardial sensitivity to or excessive production of catecholamines; an abnormal hypertrophic response to myocardial ischemic, fibrosis, or trophic factors; a primary collagen abnormality; or abnormalities of the myocardial calciumhandling process. Some cats with HCM have high serum growth hormone concentrations.

Secondary Hypertrophic Myocardial Diseases

Myocardial hypertrophy develops as a compensatory response to certain identifiable stresses or disease; marked left ventricular wall and septal thickening and clinical heart failure can occur in some cats. Such cases are not considered idiopathic HCM. Secondary causes should be ruled out if left ventricular hypertrophy is identified.

Testing for hyperthyroidism is indicated in cats with myocardial hypertrophy that are 6 years of age or older. Hyperthyroidism alters cardiovascular function by its direct effects on the myocardium and through the interaction of heightened sympathetic nervous system activity and excess thyroid hormone on the heart and peripheral circulation. Cardiac effects of thyroid hormone include myocardial hypertrophy and enhanced heart rate and contractility. The metabolic acceleration accompanying hyperthyroidism creates a hyperdynamic circulatory state characterized by increased cardiac output, oxygen demand, blood volume, and heart rate. Systemic hypertension can result and further stimulate myocardial hypertrophy. Clinical cardiovascular signs often include a systolic murmur, hyperdynamic precordial and arterial impulses, tachycardia and arrhythmias, and evidence of left ventricular enlargement or hypertrophy, seen on electrocardiograms (ECGs), thoracic radiographs, or echocardiograms. Signs of congestive heart failure develop in an estimated 15% of hyperthyroid cats; most have normal to high fractional shortening, but a few have poor contractile function. Specific therapy, in addition to the antithyroid treatment, may be necessary to manage the cardiac complications of hyperthyroidism. ß-Blockers can temporarily control many of the adverse cardiac effects of excess thyroid hormone, especially tachyarrhythmias. Diltiazem is another alternative therapy. Treatment for congestive failure is the same as that described later for HCM. The rare hypodynamic (dilated) cardiac failure is treated in the same way as dilated cardiomyopathy. (ß-Blocker or other cardiac therapy is not a substitute for antithyroid treatment, however.

Left ventricular concentric hypertrophy is the expected response to increased ventricular systolic pressure (afterload). Systemic arterial hypertension  increases afterload because of high arterial pressure and resistance. Increased resistance to ventricular outflow also occurs in the presence of a fixed (e.g., congenital subaortic stenosis) or dynamic left ventricular outflow tract obstruction. The latter occurs in some cats with idiopathic HCM and is described later.

Cardiac hypertrophy also develops in cats with hypersomatotropism (acromegaly) as a result of growth hormone's trophic effects on the heart; congestive heart failure ensues in some of these cats. Increased myocardial thickness occasionally results from infiltrative myocardial disease, most notably from lymphoma.

Pathophysiology (Diastolic Dysfunction)

The myocardial thickening that occurs in HCM leads to increased ventricular stiffness and the development of relaxation abnormalities. Left ventricular filling is impaired and higher diastolic pressures are required when the ventricle is stiff and less distensible. Furthermore, the myocardial relaxation process may be prolonged and incomplete, especially if the myocardium becomes ischemic. Fibrosis and disorganized myocardial cell structure can also contribute to the development of abnormal ventricular stiffness. Because progressively higher filling pressures are required as the left ventricle becomes more stiff, left atrial and ventricular enddiastolic pressures rise. The atrium enlarges, sometimes markedly, but the left ventricular volume remains normal or decreased. A reduced ventricular volume results in a lower stroke volume and may contribute to the activation of the renin-angiotensin system and sympathetic nervous system. Geometric changes of the left ventricle and papillary muscles or abnormal (anterior) systolic motion of the mitral valve may prevent normal valve closure. The resulting mitral regurgitation exacer bates the increased left atrial volume and pressure and may lead to pulmonary congestion and edema. Higher heart rates further interfere with left ventricular filling, exacerbate myocardial ischemic, and promote venous congestion by shortening the diastolic filling period. Contractility, or systolic function, is usually normal in affected cats.

 

 

 

 

 

What is hypertrophic cardiomyopathy?

Hypertrophic cardiomyopathy (HCM) is the most common heart disease of cats, whether they are random bred or pedigreed. It is a heart muscle disease in which the papillary muscles (the muscles in the left ventricle that anchor the mitral valve) and the walls of the left ventricle become abnormally thickened. HCM is often a progressive disease, and a proportion of affected cats develop heart failure if the muscle hypertrophy and subsequent scarring of the heart muscle significantly affects heart function. Cats with the disease may die suddenly and may develop a blood clot in the chamber above the left ventricle (i.e., the left atrium) that often then gets carried into the systemic arterial system, most commonly lodging in the terminal aorta, stopping blood flow to the rear legs. For more information on HCM, see: members.aol.com/jchinitz/hcm/index.htm

What causes HCM in cats?

This is currently unknown in most cats although familial (hereditary) HCM has been observed in several breeds, such as the Maine Coon and American Shorthair. Anecdotal information suggests there is familial HCM in many other breeds. Heart muscle hypertrophy in cats can be caused by other diseases, such as systemic hypertension (high blood pressure) and hyperthyroidism. HCM is a primary disease of the heart muscle. Hypertension and hyperthyroidism cause secondary thickening of the left ventricle and so are not causes of HCM (although it is possible that they may exacerbate the disease if they become present in a cat with mild to moderate HCM). HCM is diagnosed when these other causes are ruled out.

Is HCM genetic?

In Maine Coons and American Shorthairs, HCM has been confirmed as an autosomal dominant inherited trait, as it is in humans where over 200 gene mutations in 10 genes have been found to cause the disease. The disease has variable expression; meaning some cats are severely affected, others are only mildly to moderately affected, and some cats may not have evidence of the disease yet produce affected offspring. Recently, a mutation in the cardiac myosin binding protein C (cMyBP-C) gene causing HCM in the Maine Coon cat has been identified. doubtedly, other mutations responsible for HCM in cats remain to be discovered. However, since few veterinary cardiologists and geneticists have the expertise to study genes, it may be some time before the responsible gene or genes for each affected breed will be found. The mutation identified as a cause of HCM in Maine Coon cats may not be the same mutation or even on the same gene in other breeds. The genetics of HCM in each breed will require investigation of each individual breed.While a specific feline gene mutation has not yet been identified, research is underway in the Maine Coon cat. However, since few veterinary cardiologists and geneticists have the expertise to study genes, it is unlikely that the responsible gene or genes for each affected breed will be found at any time in the near future. If a gene is identified as a cause of HCM in Maine Coon cats, it may not be the same gene responsible for HCM in other breeds. HCM will require investigation in each breed individually.

Can HCM have a nutritional cause?

There is no evidence in cats, humans or other species of animals that HCM can have a nutritional cause. Some researches show raw food diet may have some connection with HCM. More research is needed.

How is HCM diagnosed?

HCM is diagnosed using ultrasound of the heart – an echocardiogram. Echocardiography is a good way to detect moderate to severely affected cats. However, it may not always detect mildly affected cats where changes in the heart can be minimal. Ideally, an echocardiogram to test cats for HCM should be performed by a board-certified cardiologist or radiologist. In addition to an echocardiogram, other tests may also be useful in assessing cats with HCM. For example, a chest x-ray is necessary to detect heart failure in cats with severe HCM. An electrocardiogram is useful in cats that have abnormal heart rhythms. Blood pressure measurement and blood testing for hyperthyroidism are indicated to rule out other diseases that mimic HCM, especially mild to moderate HCM. A genetic test is now available for the known cMyBP-C mutation causing HCM in Maine Coon cats. The test is available from the Veterinary Cardiac Genetics Lab of Dr. Kathryn Meurs at the College of Veterinary Medicine, Washington State University (http://www.vetmed.wsu.edu/deptsvcgl/). The test can identify which cats have the mutation. If a cat is identified as having the mutation, the test can also determine whether the cat carries one copy of the gene (a heterozygote) or two copies of the gene (a homozygote).

Should my cats be tested for HCM and how often should they be tested?

In clinical practice, the most common patients tested for HCM with echocardiography are cats with suggestive clinical signs of heart disease, such as a heart murmur. Testing cats used in a pedigreed breeding program is a more difficult endeavor. Echocardiography is not a perfect tool for diagnosis of HCM – some affected individuals will escape detection and access to good quality ultrasound services may be difficult and expensive for some breeders. At the very least, breeding cats should be ausculted (examined by a vet with a stethoscope) for heart murmurs or arrhythmias once yearly. Any cat with an abnormality should have an echocardiogram. A significant percentage of cats with HCM will not have a heart murmur, however. Since HCM can occur at any age, a single normal echocardiogram does not guarantee a cat is free of disease. Breeding cats should probably have an echocardiogram yearly during their breeding years. Examining retired cats periodically is also advantageous as this may allow the identification of affected cats that have offspring in a breeding program. A Maine Coon cat that tests negative for the cMyBP-C mutation is not guaranteed to be free of HCM, for it is not known if other mutations causing HCM are present in this breed. Ideally, cats that test negative for the cMyBP-C mutation should still undergo echocardiogram screening. Cats that test positive for the disease should not be bred. They will most likely develop the disease at some time during their life although it may be too mild to detect even on an echocardiogram.

At what age should a cat be tested for HCM?

HCM can affect cats at any age. It has been seen in kittens only a few months of age and in cats over the age of 10. In Maine Coons, most affected male cats have evidence of disease by 2 years of age, and most affected females have evidence of disease by 3 years of age although instances have been documented where the disease has not shown up until much later. Ragdolls with severe disease seem to develop it earlier in life, often at under 1 year of age. Guidelines for other breeds have not yet been developed. It is therefore hard to recommend a specific age to start testing. It may make sense to screen most breeding cats with an echocardiogram for the first time around the age of 2 years. Maine Coons may be tested for the cMyBP-C mutation as kittens.

What do I do if my cat is diagnosed with HCM?

The cat should be removed from the breeding program and all offspring should be watched closely for the development of HCM. Statistically, 50% of the cat’s offspring would be expected to have the genetic mutation that causes HCM if one parent was a heterozygote. However, the most prudent approach may be not to use any of the offspring in a breeding program. The offspring of Maine Coon cats with the cMyBP-C mutation should be individually tested to determine their status. The parents of an affected cat should also be examined with echocardiography (and tested for the cMyBP-C if a Maine Coon), as one of them likely carries a gene mutation for HCM. In some cases, identification of the affected parent may be difficult, especially if the disease is mild. In these cases, the most prudent approach may be to remove both parents from the breeding program. It is possible for a cat to develop a spontaneous mutation that causes HCM during embryonic development but this is an unlikely cause in a breed known to have the problem. All breeders that are using cats related to an affected cat should be notified that a cat has been diagnosed with HCM. Similarly, pet owners should be notified that a relative has been diagnosed with the disease. Echocardiographic examination (and genetic testing if a Maine Coon) of cats related to the affected cat should be performed.

Will we ever eliminate HCM from my breed?

The tools we currently have to diagnose HCM (i.e., echocardiography and necropsy) are not perfect and will not allow us to totally eliminate this disease. However, echocardiographic screening will be able to reduce the incidence of HCM within a breed if enough breeders are involved. The identification of the cMyBP-C mutation in the Maine Coon and the development of a genetic test provide breeders with a new tool to reduce the prevalence of or theoretically eliminate the mutation within this breed by not breeding affected cats. Breeders should use all the information they can gather about HCM in family lines, including pedigree analysis based on accurate identification of affected cats. Any cat that dies suddenly or dies from HCM should have a necropsy (i.e., post mortem examination). Most cats with HCM will have a heart that weighs more than 20 grams and most cats with severe HCM will have a heart that weighs more than 30 grams. Myocardial fiber disarray, the hallmark microscopic heart muscle abnormality seen in humans with familial HCM is seen in all Maine Coon cats with HCM. Unfortunately, most veterinary pathologists are not trained to recognize this lesion. In the long term, we will need a genetic test for HCM in each breed. A genetic test allows us to identify affected cats before they were bred and do so accurately. Since the disease is inherited as an autosomal dominant trait, once a mutation is identified, if all breeders cooperated by testing their breeding cats for the mutation the disease could be eliminated from the breed within several generations. However, the money and resources necessary to identify the gene or genes and to develop a genetic test for each breed are scarce in veterinary medicine. Breeders and cat fanciers can help by supporting research through organizations such as the Ricky Fund established by the Winn Feline Foundation.

Can two normal parents produce a kitten with HCM?

Since HCM is known to be an autosomal dominant trait in the breeds where the inheritance is known, each affected cat must have one affected parent. However, there are possible situations in which an affected cat may come from two apparently normal parents. The first possibility is that one of the parents has been misdiagnosed. This can happen due to inexperience of the ultrasonographer or poor quality equipment. It can also happen if a cat’s status is decided on the basis of only one or two ultrasounds early in life. Since HCM can develop at any age, a cat that is normal on ultrasound one year could still have HCM and show signs later in life. Since the trait has variable expression, not every affected cat will have echocardiographic evidence of HCM. It is therefore possible for a cat to test negative for HCM on ultrasound, and yet still carry a genetic mutation and pass it to offspring. Finally, it is possible for spontaneous mutations to occur in cats from normal parents. These cats may then pass on their mutation to offspring. We do not know how often spontaneous mutations causing HCM occur in cats. Statistically, spontaneous mutations are more likely to occur in random bred cats than in pedigreed cats.

What does "HCM free cattery" mean?

There is no universally agreed upon definition of an HCM free cattery. The terminology is currently unclear, as different breeders mean different things when they use this term. Ideally, each breed should develop a specific definition and guidelines for use of this designation for catteries.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Information provided by RainbowSafariBengals