| I have done a lot of research on rat genetics and come up with some of my own assumptions. Anyway, here are my findings. My resources include clubs, breeders, and my own deductions based on others' breedings as well as my knowledge of other animals' genetics. Most of my knowledge of basic genetics comes from high school biology books I read as a child (in elementary school) as well as my introductory undergraduate biology class. What I know of rat genetics, I found on the internet. Here are some of my resources: |
(Note the key scientific terminology in bold print. Check the glossary for definitions.)
Genetics is a word that scares people. It sounds like a really tough subject. No one (except nuts like me) would want to learn/discuss genetics for fun. Genetics can be complicated on some levels, talking about DNA structure, meiosis, how and why mutations occur... BUT I'm not going to discuss any of that here. For a breeder or any person interested in inheritance, you only need to understand Mendelian genetics (also called "Classical" or "Transmission" genetics).
You can learn about Gregor Mendel from pretty much any Biology book or a web search. He was a monk who cross bred pea plants and discovered the nature of how many traits are inherited, and about dominance and recession of genes. The basic ideas are:
Here are some other sites where you can learn the basics of Mendelian Genetics (all animals follow the same scheme of inheritance):
Mendelian genetics really simplify inheritance. In truth, some genes are linked to each other. (Human beings have only 23 pairs of chromosomes, for instance, but many thosands of genes.) Also, genes and DNA are nothing more than "instructions" for an organism's body. Sometimes one effect will interact/conflict/change another. In addition, looking at the organism as a whole is much more complicated than just looking at the probabilities and effects of a single gene. I'll present here only the extensions that any breeder should know and be comfortable with. Please look to other sources for more in depth genetics info. (It is fascinating!)
Not all genes are simple recessive/dominant. A gene can have any number of alleles (which on a molecular level can be a variation in a single base pair, of which a gene contains many). Some gene pairs work on different levels of dominance, but others have a semi-dominant relationship. One example is a rat with two siamese genes is siamese c(h)c(h). One with two albino genes is albino cc. However, a rat with one albino gene and one siamese gene is neither phenotype, but a third "in-between" one called himalayan. and a full color gene "C" is dominant to both other alleles, so CC, Cc, and Cc(h) all have the same phenotype.
In addition you need to think about how two or three or more pairs of genes wiil affect each other. Here is one example of phenotype for multiple gene pairs: "aa" is non-agouti, "rr" is fawn, and "gg" is blue. A rat that is "aarrgg" is not black, fawn, or blue, but the result of all the effects interaction: platinum. The non-agouti removes the color bands on the hairs; the fawn genes dilute the fur and eye color, and the blue dilutes it further. Many rat varieties are the results of these sorts of interactions.
In some cases, genes interact through an epistatic relationship. Epistasis means that one gene pair essentially "overrides" another pair. It is sort of like dominance, but involving one pair relating to another rather than alleles in a single pair. The most classic example is albinism. Any rat that is "cc" is albino regardless of any other color or marking genes. (The reason this is is that the albino mutation prevents the rat from developing pigment, so no matter what pigment the rat is "coded" for, it just won't develop.)
Another consideration is sex(gender)-linkage, which applies to any gene inherited on the sex chromosomes (most commonly the "X" chromosome, but can occur on "Y" too). Sex linkage of color/marking/type mutations in rats is not well known or common, so usually doesn't need to be considered. If you are interested in learning about it, look up the yellow/brindle genes in mice, the red/calico genes in cats, or drosophila genetics.
Finally, there are the "lethal genes." No, a gene cannot kill someone. It is just an instruction for the cells. However, some of the effects cause a rat to die before reaching reproductive maturity or often before birth. Fatal genes often simply signal an egg cell or fetus not to develop at all or to be aborted in early stages. Many genes have "harmless" effects when heterozygous (the two alleles are different) but are fatal when homozygous. One example is the pearl gene. In rats, "Pepe" is pearl. When there are TWO pearl genes (PePe), however, the fetus is aborted in early stages and reabsorbed by the mother. You see no effect from this because no baby is born at all, which leads to a smmaller litter. (Some "fatal" genes involve a live birth but death within a couple weeks.)
As long as you remember that each gene pair in inherited independently of other genes (with the exception of linked genes, but you don't have to worry about that for most things), and that every baby produced in a cross randomly (50/50 chance for each gene)inherits one gene from mom and a random one gene from dad, predicting the babies is very simple. It can be drawn out using Punnet Squares.
Here's how you draw Punnet squares.
Here are some examples of Punnet squares for crosses between blue rats (blue being recessive) and black rats (some carrying blue and some not). We're assuming all rats involved are aaHH.
Recessive x Dominant(carrier)
Dominant(carrier) x Dominant(non-carrier)
Dominant(carrier) x Dominant(carrier)
Recessive x Recessive
There are many known alleles of many rat genes. Breeders mostly focus on the color and type and other physical traits (not that they are more important, but because they can be SEEN). The other genes are important to be aware of, but I myself am not experienced with them. Here is the site that I think has the best overview of known rat genes and their effects: Rodentfancy Rat Genetics Page
Here is a list of agouti (ticked) colors and their genotypes. Most colors have been scientifically described (meaning their letter designations and nature are documented); others are assumed or known by breeders. A "-" means that any allele can be there (so it is a dominant trait). Also, notice that some genes are designated with two letters (like "si" for silver.) I include only the gene pairs that affect each color. Assume all other genes have no mutation (which is almost always dominant to mutations--they may CARRY recessives).
Agouti: A- (no mutations/recessives): This is the "wild color." Agouti rats have black/yellow/brown bands on their fur and grayish stomachs. Appearance is similar to a ticked tabby cat (appears chestnut brown from a distance).
Chocolate Agouti: A-bb: Like agouti but a richer brown with little or no black.
Russian Blue Agouti: A-dd: A rat with Russian Blue (gray) and creamy yellow ticking.
Blue Agouti: A-gg: Also known as "opal." Similar to Russian Blue agouti but lighter colored.
Cinnamon: A-mm: A light brown agouti, like chocolate agouti but not as rich.
Classic Lynx: A-bbdd: An agouti form of classic lilac.
Fawn: A-rr: An orange color with a lighter belly. Eyes are a dark ruby color (they may look black in indoor lighting).
Silver Fawn: A-rrsisi: Like fawn but with 50% of guard hairs white
Amber: A-pp: Yellow to gold in color with a creamy colored belly. Eyes are pink to red in color.
Topaz: A-mmrr: A less orange version of fawn.
Cinnamon Pearl: A-mmPepe: A light brown agouti, like chocolate agouti but not as rich. (Note: "PePe" is lethal in utero, and rats with this genotype are reabsorbed before they are born.)
Other agouti colors can be found. They are essentially ticked versions of non-agoutis.
Here is a list of non-agouti colors and their genotypes. Most colors have been scientifically described (meaning their letter designations and nature are documented); others are assumed or known by breeders. A "-" means that any allele can be there (so it is a dominant trait). Also, notice that some genes are designated with two letters (like "si" for silver.) I include only the gene pairs that affect each color. Assume all other genes have no mutation (which is almost always dominant to mutations--they may CARRY recessives).
Black: aa: Dark, pitch black.
Silvered Black: aasisi: Black with 50% of guard hairs white.
Chocolate: aabb: Rich, warm brown.
Russian Blue: aadd (sometimes "rb" instead of "d"): A cool medium gray color.
American Blue: aagg: Also called blue, sky blue, or slate. A cool light gray color.
Russian Silver: aaddgg: A very light silver. Eyes are black.
Mink: aamm: Medium brown, a colder hue than chocolate.
Coffee: aabbmm: A tan brown that looks like coffee with cream.
American Lilac: aamm + modifiers: A light form of mink.
Classic Lilac: aabbmm: A warm gray color, like that seen in other animals (lilac cats, for instance). Eyes are black.
Beige: aarr: A cream color from yellow to a dull khaki or even orangish. Eyes are dark ruby and may look almost black.
Champagne: aapp: A light, creamy yellow color. Eyes are pink to red.
Buff: aammrr: A lighter, warmer beige.
Blue-Beige: aaddrr: A tan color with a blue-gray tint. Eyes are dark ruby and may look almost black.
Platinum: aaggmm or aaggrr: A silver color not as light as Russian Silver. RED-based platinums may have reddish eyes.
Silver: aaggpp: An off-white color with an ice-blue hue. Eyes are pink.
Ruby-Eyed Mocha: aammRr: A coffee color with a red tint to the eyes.
Pearl: aammPepe: A very light gray/silver with black eyes. Also associated with merle. (Note: "PePe" is lethal in utero, and rats with this genotype are reabsorbed before they are born.)
Black-Eyed White: See the markings section. BEW are not known to be the result of color mutations or albinism, but rather are from high white markings.
European Husky/Roan: Uncertain genetics but believed to be a simple recessive. "True" huskies exist only in Europe. It is also called roan but is not like roans in America. It is a mixture of white hairs, both undercoat and guard hairs, and the color fades drastically with age, making all but vary dark colors appear white. (In the US, we have some fading and marking genes that we call "husky" or "roan," but they are different.)
American Husky/Roan: Uncertain genetics, but related to white spotting genes. Several types of fading genes are found in the US, and many are associated with the fatal condition megacolon (often not as a result of a certain fading gene but rather crossing lines with different genes that are essentially "incompatible").
Charcoal: aa(+modifiers): Seen in some lines of white marked rats, a gray that results from black being "muted" by white marking genes.
Siamese & Albinism
The "C" locus includes a variety of genes that cause albinism or partial albinism. Albinos are animals that lack pigment in skin, fur, and eyes. Siamese and other "pointed" animals have the pigment reduced or missing but present in the cold parts of their body, which includes ears, nose, feet, tail, and , to a lesser degree, the lower back. This kind of coloring should not be confused with "marked" varieties (rats with white markings on them). All of these rats can have white markings. In the case of an albino, you won't know from looking, of course, but the rat can be genetically hooded or capped while still being albino. White-marked siamese are sometimes called "trimese" or "snowshoe." They often have white gloves or even all their dark points masked by white markings.
Albino: cc (and any other genes): White rat with pink eyes. (Note: Pink-eyed white rats can also be a result of markings and/or the presence of several color dilution genes.)
Seal-point Siamese: aac(h)c(h): Eggshell/off-white body with dark brown to black on "cold" areas, the nose, ears, feet, and tail. (Note: a siamese with white markings such as hooded or capped may not show all the brown points because of the white. Also, agouti genes "wash out" the points, making them lighter.) Eyes are medium red to ruby.
Blue-point Siamese: aaggc(h)c(h): Siamese rat with blue points and light body. Eyes are medium red to ruby.
Russian Blue-point Siamese: aaddc(h)c(h): Siamese rat with Russian Blue points and light body. Eyes are medium red to ruby.
Mink-point Siamese: aammc(h)c(h): Siamese rat with lighter brown points and body. Eyes are medium red to ruby.
Himalayan: cc(h): Rat with a white body and light "siamesish" points. Points do not extend as far as in a siamese. Eyes pink in color (like an albino). Himalayans can be seen in many colors, as siamese can. White markings can disrupt or hide color points.
Burmese: c(h)c(b): The burmese gene is not officially described (I'm calling it "cb"). This variety currently exists only in Europe. Burmese rats have darker bodies and points than siamese (like burmese gerbils or cats).
Black-eyed Siamese: cc(e): Another new and currently only European variety. A siamese rat with black eyes.
Black-eyed White: See the markings section. BEW are not known to be the result of color mutations or albinism, but rather are from high white markings.
Here is a list of fur types and their genotypes. Many genes have been scientifically described (meaning their letter designations and nature are documented); others are assumed or known by breeders. A "-" means that any allele can be there (so it is a dominant trait). Notice that many fur mutations are designated by two or three letter notations; don't be confused. "Re" is one gene just like "A". Also realize that some types can look very similar but have different genetics, and it is not certain if different rexes are actually caused by different genes, but you can still use this list for practical purposes. Rats of ANY color or marking can have any fur type. As far as I know there are no genetic links between specific colors and specific types.
Standard: no mutation: Typical rat fur. Straight and medium in length. There is short fur on the stomach and longer fur on the back. Guard hairs in males are a little coarser than in females.
Teddy Rex: Cu1cu1 or Cu2cu2: Fur is soft and wavy with curved to curly whiskers. Can look and feel feathery. Only seen in the US, though similar rats in Europe may be considered "poor Rexes." Also called velveteen.
Rex: Rere Curly fur with reduced guard hairs. Whiskers are curly.
Double Rex: Cu1Cu1 or Cu2Cu2 or ReRe: Whiskers and fur very curly and short. Can look like poodle fur. Rat may look shorn and/or may have bald patches or be nearly completely bald at points in its life. Also called patchwork hairless. Double Rexes can vary a lot in their texture and appearance.
Hairless: fzfz or shn/shn or rnu/rnu or hrhr: Hairless rats are, well, bald. Some hair may exist on face and pubic areas. Whiskers are short and curly.
Velvet/Velour: kk: Fur and whiskers are short and crimped or twisted. Very reduced to no guard hairs.
Satin: Genetics are unknown. Fur is very soft and shiny and may look longer than a standard coat (if only because it lies flatter).
Here is a list of body/ear types and their genotypes. Many genes have been scientifically described (meaning their letter designations and nature are documented); others are assumed or known by breeders. A "-" means that any allele can be there (so it is a dominant trait). Some body types are new or controversial (as most new things are). It is not well known if any of these types are genetically conflicting with each other because only standards and dumbos are well-developed and widespread, but they should all be able to occur in any color, marking, and/or fur type.
Standard: no mutation: "Normal" rat. This is the body type that occurs in the wild (well, sort of, domestic rats have been bred larger with appealing faces and longer tails).
Dumbo: dudu: Ears are set on the sides of the head, pointing more horizontal than vertical. Ears also are larger than standard ears and are rounder (standards have "tulip" ears). Head may be wider and flatter than a standard and the body may be stockier.
Tailless: Tal- or stst: Tail absent. Hind legs are lengthened and rat has a round look like a rabbit. "Tailless" rats vary a lot and can have spinal problems or not be able to give birth. "Rumpies" are completely tailless. "Stumpies," "risers," and "shorties" have varied tail lengths. A well bred tailless rat should have no spinal irregularities, oddities to his gait, or balance problems. Only people VERY experienced with rats and knowledgeable about genetics should breed tailless rats.
Dwarf: There are many dwarfing genes. Most cause sterility or other problems. Most (if not all) are recessive. Dwarfing genes usually cause heads to look larger and bodies to be more compact.
Markings are quite complicated, and since they are the focus of one of my lines, I have a lot to say about them and am in progress of finding the nature of the ones in my lines. Because of this, markings are discussed on their own page
Odds & Ends
There are other colors being developed and other genes that are known to cause color or marking types. I'm listing here some of the minor genes as well as some observed new varieties and the theories of their genetics. (And some other lesser known genes too.)
Head Spots and Blazes: There are a variety of ways facial markings are formed. There is a recessive head spot gene wih hshs causing a spot that can be very small or very large in different shapes. Some blazes are the result of head spots that are elongated. Many of these are uneven, often going from the forehead to the side of the nose. There are other causes too. Blazes are associated with husky genes and a headspot may result from the h(n) gene too. Some blazes can be inherited dominantly or in connection with other genes.
Odd-eyes: Odd-eyed rats are those with one eye a lighter shade than the other. (Rat eyes run the range from black through red to pink.) Odd-eyes are not controlled by a single gene but rather are associated with certain white marking genes, especially those that are asymmetrical. "Double odd-eyes" can also occur, in which both of a rat's eyes are lightened, making red-eyed rats in colors that should be black-eyed (like blacks, blues, and agoutis). Although they are associated with marking genes, odd-eyed solid rats have been documented. Any odd-eyed rat, should be considered "high-white" and may be a megacolon risk.
Tricolors/Mosaics: A tricolor is an animal that has white on it in addition to two other colors. There are a few types of "tricolors" that occasionally show up.
Sand Locus: These genes are documented but rarely seen in real life. A simple recessive sdsd fades agouti to brown-yellow, and black to dark gray. Its effects on other colors is uncertain.
Smoke: There are some rats that look like smoke cats. Smoke in cats is caused by a dominant gene, but in rats it is believed to be a recessive smsm. It may be a variation of silvering genes.
Conditions and Debilitations
Mutations can occur anywhere on a DNA strand. In most places (for rats and people anyway) this has no effect and produces normal individuals. Other mutations cause the first mutated cell to die immediately and not reproduce at all. Because this is random (and rare), mutations only occasionally make desirable and attractive effects like new colors and types. It can also cause deformities and genetic conditions like megacolon and diabetes. By understanding the genetics of existing inherited problems, breeders can avoid them and develop healthy lines.
Zucker's Syndrome: The recessive genes fafa cause very obese, fatty rats. Zucker rats cannot "lose weight." They are usually diabetic and die young.
Diabetes: Obesity can be related to some types of diabetes. Most forms of diabetes are recessive. One gene is designated "di"
Fatal and "Dangerous" Genes: Pearl, many white marking genes, and some dwarfing and fur type genes are fatal or linked to other problems. Hairless rats have a number of problems associated with different genotypes from dental malocclusion to kidney failure and other problems. (See the link at bottom of this page.) There are a number of recessive rexing/fur genes that result in seizures or other problems (these are mostly genes found in laboratories, not in the pet trade). Taillessness has some serious problems correlating to the changes in the spine/nervous system.
Megacolon: Megacolon is a disorder where at a stage in the embryo's development, the nerves for the colon do not form connections properly. Rats with megacolon cannot properly move their bowels and usually die very young (under 10 weeks old). It is linked to some white marking because of the place on the spine that megacolon affects (it correlates to the spread of color on the rat). The spotting lethal gene that causes one form of megacolon is a simple recessive: slsl However, megacolon may also result from combinations of other spotting or fading genes. Please read this page for more information about megacolon and white markings.
Cancer: It is known that cancer can have hereditary influences, but the exact nature of these influences is unclear. Mutations on oncogenes are responsible for several forms of cancer. (Oncogenes are genes that are code for cell grown and regulation.) Breeders are working towards cancer-free lines by keeping good records and staying in touch with adopters on the health of the rats they place.
Allergies and Vulnerabilities: Allergies and sensitivities to dust, stress, and infection have been known to be slightly to strongly hereditary. The nature of the heredity is not clear, so dedicated and responsible breeders watch their rats' health closely, breed rats older (usually no earlier than six months for females and even waiting for over a year for males), and breed only rats that are in the best health. (Behavioral problems have also been known to be hereditary, so it is not a good idea to breed "biters" or skittish rats.)
Historical Note: While it was being developped, the "English Blue" variety had serious hemmoraging problems that killed rats when they gave birth. Those problems were "bred out" of the blue line. It is possible to "breed out" some problems that are not too strongly linked to a certain variety nor too detrimental to the line as it is being developed. For example, many hairless lines are fairly long-lived and do not suffer the inability to lactate that is commonly seen in the variety. The more we know about linkage and the nature of the heredity of traits, the better chance we have of elliminating these problems and improving out pets' health and longevity.
Specific Genetics/Heredity Articles
Here are some helpful articles on breeding and heredity (I didn't make any of them):