GENETICS OF BENGAL CATS

Hello, have you ever wondered which is the difference between a solid and a tabby cat? what it means dilute or agouti? Which is the way you can transmit the ''snow'' and the charcoal gene? (Tou have to know the mendel's characters transmissions to understand below). I have written this with a simple graphic to permit yout to understand this argument, i have put not only the teory but even the images of the difference between the bengals' colors. Just watch the images if you are not the person who like to read, i think they are intuitive.

Tabby means ''spotted/striped and genetically is when the single hair has some bands (opposite is solid with no bands) that will lead to different patterns. (mackerel, spotted, classic and ticked). If a cat has the agouti gene (alleles: AA) phenotipically (phenotype is the appearence) will be Tabby.

If the cat is non-agouti (aa) phenotipically will appear solid, so Black aka melanistic.

If a cat instead is Aa means that he is non -agouti carrier but phenotipically will appear tabby.

Black and tabby is the same color but expressed with different patterns.

A melanistic colorpoint will not appear black, check down below.

Inhibitor gene (SILVER)

Silver cats has the inhibitor gene, that will turn the warm color, the agouti part, to white. So the undercoat will be completely white with black spots/stripes and a complessive color grey. If the cat has too much roufism you will see some brownish zones and he will appear tarnish.

To have a silver cat one of the parents must be silver.

II = Homozygousinhibitor gene, all offspring will be silver.
Ii = Heterozygous inhibitor gene, 50% offspring will be silver.
ii= No inhibitor gene, the cat will have silver offspring only if mated with a silver

Colorpoint and Burmese (SNOW)

Colorpoint is a kind of albinism, the points of the cats exposed to cold will become darker (termic color) it is known as hymalaian gene and probably bengals got it from siameses. The burmese color (sepia) instead comes for sure from burmese breed. Breeding a colorpoint cat to a burmese cat you will have tonkinese color.

Simply:

siamese gene = Blue eyes, lighter coat.
tonkinese gene : Acqua eyes, middle shade color.
burmese gene = gold-green eyes, darker color.

Snow Lynx has then siamese/colorpoint gene, Snow Mink bengals has Tonkinese gene and Snow Sepia bengals has burmese gene.

This color is recessive so to have a Snow bengal you need snow parents o snow carrier parents. Colorpoing kittens will born completely white.

Breeding two colorpoint will lead to better and deep eye color

DILUTED

Two copies of the diluted gene, will make appear a black cat, blue and a red cat, cream.

Black (B) can be chocolate (b) o cinnamon (bl) depenting on the pigment shape that will reflect light differently showing us different phenotipic colors. So in order a black cat with dilute gene will appear blue, a chocolate cat will be lilac and a cinnamon cat will be fawn. Two copies of allele D (DD) means that the cat is not dilute.. Dd means the cat is carrier of dilute gene but it is not dilute and dd means the cat is dilute.

Blue bengals than are dilute and own an homozigotous copy of dilute gene.

AGOUTI/TABBY: NON-AGOUTI/SOLID:

CHARCOAL

In a completely different section we have Charcoal bengals (apb/a), they eredited apb gene directly from ALC and non-agouti gene by domestic cats. The difference from melanistic bengals is that Charcoals have more contrasted spots, white goggles (contour of the eye), a black stripe that run their back called cape and a black mask on their face a lor more visible on snows.

Silver Mink Charcoal Spotted - FLAMING ICE NORTH of BENGATTO:

Genetic Diseases

HCM- Hypertrophic cardiomyopathy
Pk-def
Pra-b
Flat chest and Escavatum sternum

HCM

CARDIOPATHY: indicates a generic group of pathologies affecting the heart e.g. valve diseases (stenosis, insufficiency, prolapse), heart failure, arrhythmias (extrasystoles, tachycardias), heart attacks
CARDIOMYOPATHY: refers specifically to pathologies affecting the myocardium, ex: the heart muscle.

CONGENITAL heart diseases are malformations of the heart structure or circulatory function, present since birth. Among these is hypertrophic cardiomyopathy (HCM) (ventricular thickness), which results in a thickening of the myocardium and the walls of the left ventricle with consequent less blood flow.

HCM has a prognosis of 4/5 years if treated in the asymptomatic phase, 6/12 months if in the phase of decompensation.
Symptoms: lethargy, increased respiratory rate, loss of appetite and weight.
It is essential to exclude the use in the reproduction of clinically ill subjects. For this reason, a control echocardiogram must be done every 12-18 months on all breeding animals.

Ps: some cardiomyopathies can be caused by a deficiency of taurine. Integration takes months to reverse the process

Pra-b

Bengal PRA-b causes loss of photoreceptors in the eye and ultimately results in blindness. Clinical signs typically become evident between 8 and 20 weeks of age and the disease progresses so that by around one year of age complete retinal degeneration is apparent in most cats1. At this age the affected cats also show behavioural signs of blindness. Affected cats can have more difficulty at night, their pupils are usually more dilated and they show marked tapetal hyperreflectivity1. As with blind cats in general, PRAb affected Bengals can negotiate their home environment relatively easily and are mobile and active. The mutation is inherited as an autosomal recessive trait, meaning that cats with only one copy of the mutant gene (Heterozygous or Carrier) have normal vision, but they can pass the mutation to their offspring. Cats with two copies of the mutant gene (Affected) will develop PRA. We have screened nearly 2500 Bengal cats from across Europe and found Carriers in most European countries (see table below). The overall European Bengal PRA-b Carrier prevalence is around 18%.

Pk-def

Pyruvate kinase deficiency is an inherited disease of Abyssinian and Somali cats. Pyruvate kinase is a red blood cell enzyme important in red blood cell energy metabolism. Therefore, if this enzyme is lacking, a haemolytic anaemia can result. However, the anaemia may only be mild and intermittently detectable, or may not become evident until the cat is older. A rapid severe life-threatening anaemia can also develop. The disease is inherited as an autosomal recessive trait, so only cats with two copies of the defective gene are affected. Carrier cats are clinically healthy but can pass the defective gene to their offspring. Because initial clinical signs can be mild or go unnoticed, Affected cats may not be identified until after they have had large numbers of offspring. it comes from domestics.

These graphs are valid for all recessive diseases, including Pkdef and Pra-b:

Flat chest and sunken sternum.

Illness lethal or impairing, probably autosomal recessive influenced by environmental factors

The kitten's chest appears concave, compressed or flattened instead of convex. Spine may be depressed towards the ground. Reduced chest volume causes problems breathing and fast breathing rate. In mild cases, the flat-chested appearance is slight or intermittent and kittens are bright and active. In more severe cases kittens have breathing difficulties, are distressed, have stunted growth and may die. Internal organs are dislocated (severity depends of degree of flat chest). Mildly affected kittens can recover and the chest appears to become less obvious as they grow suggesting the ribcage muscles are involved rather than a skeletal defect, instead excavatum sternum is skeletal and probably it is not hereditary but caused during pregnancy. You can help a flat-chested kitten with some home made tutors for example with paper-rolls, search on internet for tutorials.

GENETICS OF BENGAL CATS

AGOUTI/TABBY: NON-AGOUTI/SOLID:

Genetic Diseases

HCM- Hypertrophic cardiomyopathy

Pk-def

Pra-b

Flat chest and Escavatum sternum

Pra-b

Pk-def

Flat chest and sunken sternum.