Fun with Genetics

White Spotting

Its pretty common to see cats with white markings, in all shades and patterns. This can vary from the “puss-in-boots” to nearly white cats. The primary driver of this spotting is a single gene that allows spots. The ‘volume’ of the spotting is controlled by other factors.

Buttons and Lockets

There are some white spots that are not part of the White Spotting factor. These are small spots on the chest, throat or belly on an otherwise non-white cat. While a few think this is a function of low levels of spotting, most think these ‘buttons’ and ‘lockets’ are controlled by other genes entirely. I agree, as those small spots are so common that most cats would have to have white spotting.

Julius has a ‘button’ — although it could better be called ’boxer shorts’ — a small white area on the lower stomach between the rear legs. His other ‘white’ areas – the whitish rings around the eyes (‘eyeliner’) and the whitish chin are actually part of the tabby pattern. In fact, the color of his chin is really a very very pale brown. The difference is easily apparent if you have him turned over in a good light – the button is pure white, much brighter than the chin and eyes.

If Calpurnia and Gus have a locket, it’s covered up by their true white spotting.

The White Spotting Gene

This diagram shows diagrams with the degrees of spotting, both by number and by common name. When spotting is allowed, the visual effect is very dependent on secondary ‘regulator’ genes. These act like a ‘volume control’ to the degree of spotting. The exact number and type of these regulator genes are unknown, but breeders can select for them when they are trying to fix a particular look to a cat.

The White Spotting gene is pretty simple. The dominant S gene introduces spotting. The recessive s is no spotting. The s/s combination produces no white spotting factor. Most think that S/S produces a ‘bonus’ to the spotting level, so that an S/S with regulators that would give level 2 spotting might instead be a level 3 or 4, due to the extra S However, it doesn’t seem to be the case that S/S assures you of a ‘mostly white’ cat.

The Birman cat, for example, has a requirement for white ‘gloves’ – just the tips of the feet are white. If the genetics required as S/s to achieve this, then half of all Birman kittens would be gloveless or would have too much white. Some writers postulate a ‘Birman Glove Gene’ that magically sets socks. Others deny this, and say mixing a new set of genes into Birmans disturbs the gloves until bred back true. This sounds more like the Birman breeders have bred a uniform ‘volume level’ that makes an S/S reliably produce the gloves they like to see.

The problem with such a ‘glove gene’ is that I can’t see how a cell can possibly tell its ‘on a foot’ to implement such a scheme. At the time most of this action is happening, the embryo is a glob of cells, not an itty bitty kitten that you can paint with a tiny brush.

Calpurnia and Gus are both Tuxedo White Spotted cats – around level 4. Julius does not have the white spotting gene.

White Spotting Locus Options

Gene Symbol Dominant Notes
S yes White Spotting active
s No white spotting

White Spotting Levels

The level regulating genes act like a volume control of whiteness. The white starts low on the cat – the tips of the feet and stomach, and then moving up the legs and merging along the stomach. The white then moves up the chest, to the throat and a blaze on the face.

Now we are at the Tuxedo Level. As the white spreads, the white meets over the neck first, then up the head, back, and towards the tail. Eventually the cat can be virtually entirely white. It is also possible for a cat with white spotting to show no white at all.

It can be very hard to tell the difference between a “Dominant White” cat and a “100 percent Spotted” white cat. Usually there are one or two colored hairs on a white spotted cat, that the Dominant White will not have.

How Does White Spotting Happen?

The mechanism of how the spotting works seems to be that early in the development of the embryo the ‘color control’ develops along the nerve line, what will be the spine and back. This then migrates down the sides toward the belly and where the legs and feet will form. The theory I’ve seen is that the white spotting gene makes this drift slower than normal. So if the color has not reached a part of the embryo, then it has no alternative but to be white.

Actually, I think they have it backwards, because of another side effect of white spotting – that ‘calico’ cats, that have white spotting and both orange and black, have fewer and more uniform spots, that seem cleanly separated. Tortoiseshell cats, with no white spotting have the two colors intermixed much more finely and in a more irregular way. Is there a simple way to explain this?

Remember, the pattern on these calico/tortie cats comes from X-inactivation. At some point in development, each cell ‘decides’ which X to use randomly. From then on this decision is carried down through all cell divisions after that, forming a group of cells with the same genetic pattern. In a tortie cat, one X produces orange color, the other black. So all descendants of the original decider would share the same color, forming a spot.

So if this happens when the embryo has a few thousand skin cells, there will be about this many ‘blobs’ on the adult cat’s fur when it grows up. Now lets assume that the White Spotting factor speeds up the time that this decision, and also the point when the ‘color control’ migrating down is needed. With less time to finish the migration, the color would be absent all the same, but not because of slower drift. The other effect of an earlier decision is that there are fewer cells available to form orange and black blobs in the fur, so the spots that would be fewer and more distinct.

I got this idea partly from a Stephen Jay Gould article on embryology of zebras, where a simple set of controls – form the stripes at this time, or later, coupled with the growth of the embryo fit both the number of stripes on the zebra, but how they were distributed on the adult animal. If you assumed a fixed size stripe pattern laid on top of the embryo at different points in development, everything else followed naturally to explain the stripes on different zebra species. A similar explanation fits the white spotting/calico interaction.

22 Responses to Fun with Genetics

  1. Pingback: Agouti, or not Agouti | ThreeCatYard

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  6. minlit says:

    The new analysis page is great! You’ve put so much work into it! Well done. Super project.

    Like

  7. Dianda says:

    Oh my god! Kuddo’s to you! This is great!
    Is it alright if I put this link in my blogroll?

    Like

  8. Dianda says:

    Thank you! 🙂

    Like

  9. Star Wise says:

    Wow, your genetics information is great. I have a large furry cat, Shandy, and someone said he might have Maine Coone in him. I am sorry but when I began reading your pages on coat colour I became befuddled (probably because of being tired after a hard day at work). Would you say my kitty, Shandy, is tabby and white? You can see him on “Our Animal Companions” page of my site. Thank you

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    • Oldcat says:

      Yes, Shandy is a tabby with white. The White Spotting gene is responsible for the white lying “over” the tabby pattern.
      It has a variable expression, though. For low levels this starts with white feet then moves to belly chest then face, then up the sides and around the neck. This is where Shandy is. Higher levels get to where only the top of the head and tail are non-white, then finally a completely white cat.

      I like the colored spot that still exists on the tummy, though.

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      • Star Wise says:

        Thank you Oldcat ! Your cat showcase is very pleasing and all the examples beautiful. I didn’t know there were “cinnamon” cats. I have always thought about having a blue-cream cat. My twin sister used to sketch and colour in different cat breeds, while I, more interested in “girlie” things would list all the types and brands of my cosmetics

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  10. Wonderful site! Many thanks. I do have a [few] question[s], although a bit complicated. First, I breed Maine Coons. I have a wide variety of colors, including solid white and shaded. I recently had a litter of six. The mother is solid white and the father is cream smoke shaded [possibly chinchilla, if that were recognized in Maine Coons]. The white mother is probably masking red or cream tabby or solid without white, and probably not carrying the Inhibitor gene. Of the six kittens, one is solid white. The other five, males and females, are cream silver or smoke, some probably shaded. I have been trying to determine the probability that the white kitten is masking the Inhibitor gene, with the theory [and hope] that the shaded/chinchilla father carries two rather than one Inhibitor gene. That is how I first learned about the wideband gene, which suggests that there is no way to determine whether the father carries one or two Inhibitor genes. Can you tell me if this is a correct assumption.

    Second question: I have also been trying to determine the cause of deafness in white cats. My theory, supported by some, is that the combination of the White gene and the Spotting gene is to blame. And, in a solid white cat, when the Spotting gene falls over the eye, the eye is blue. When it falls over the ear, the ear is deaf. [There are human conditions in which the lack of pigmentation is related to deafness.] Do you have any thoughts on this?

    Many thanks for your time and consideration!

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    • Oldcat says:

      Assuming Mom has no “I” genes, then if Dad had two genes all kittens would have one, which is what you see. If Dad had one “I”, then you’d expect half the kittens to be normal. So, the chance that with 50 percent per kitten you came up with all smokes is .5 multiplied 5 times, or one chance in 32 – about 3 percent. So you can’t be 100 percent confident that the all-white kitten has “I” but if you laid out all 128 choices for 6 kittens in both cases (double I dad and single I dad), then eliminated those where a visible kitten was non I, you’d find only one case out of 66 remaining choices where the white kitten has no inhibitor. Pretty good odds!

      On the second question, I’m pretty sure that dominant white OR high levels of white spotting up to the ear can cause deafness in cats, because of the link between pigment and ear development as you said. It has been a while, but I think that the Albino solid white variants (pink eye and blue eyed albino) don’t link to deafness the same way.

      I’d think that if a combination of both were required, it would be relatively easy to show it by introducing one gene or the other into a line of cats without either and showing no deafness results.

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  11. Many thanks; this is so much fun!

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  12. Star Wise says:

    Hi oldcat, I would like to ask you what you think about the genetics of Venus, the “chimera” cat, as on my Blog. Link is below.

    Also, did you ever get an email from me with a poem tribute for Gus? I tried commenting on the relevant post but Word Press wouldn’t let the Comment go through back then, for who knows what reason, so I used your Contact Me page. 🙂

    Venus – the Chimera Cat

    Like

  13. Star Wise says:

    Here is my poem tribute for Gus. I couldn’t post it on the “Farewell to Gus” thread, but you can move it to that thread if you like.

    Thank you Gus
    For transforming us
    A beautiful boy always
    You never ceased to amaze
    We loved your sweet kind face
    Your gorgeous black & white coat
    And magnificent deportment something to gloat
    Wise and special friend
    Your love never ends
    The Body goes, but the Spirit flows,
    Thank you for being with Us
    Wonderful Spirit called Gus

    Like

  14. Thank you for the accuracy and detail you have shared in your Fun with Genetics section. Cat genetics is an area that is not widely discussed but it should be.

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  15. Chris Howard says:

    I believe we just had a chimera kitten born. Mother is a dilute tortie with white feet. She had 3 dilute kittens, a tabby, a tortie, and a light gray, almost a fog color. 4th kitten is a tabby with white. The front half is normal dark, almost black tabby, the back half is dilute tabby, a light gray. I’ve never seen such a cat.

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    • Oldcat says:

      This might be a fever coat. If mother gets sick, it can affect the coat in interesting ways. Eventually the kitten fir is lost and the coat is normal.

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  16. Katie M says:

    I have two unrelated cats.

    Charlie is all black, although I can see faint tabby stripes in the right light. He also “rusts” in the sun. The strange thing about him is that the skin underneath his fur appears to be white, and the insides of his ears and mouth are very pale. I’ve had him checked out, so I know it’s not a health problem. I can’t seem to find anything on this.

    Selene is a grey tabby. She seems to have every shade of grey possible, with the lightest areas appearing either white or extremely light grey depending on lighting conditions. I even named her after an ancient moon goddess because she’s basically got all of the moon’s colors.

    Like

    • Oldcat says:

      Normal cat coloring is temperature sensitive and will be lighter near the skin. On black cats this will be a pale grey, not pink as skin is under white fur. Do a google image search on “shaved tuxedo cat” for a view of this.

      There is also a gene that blanks out the color near the skin. This produces what is called a ‘smoke’ or ‘shaded’ cat, depending on other factors. Each hair is white at the base. I don’t know if the skin is correspondingly paler to match this, but skin color does follow hair color normally.

      The rusting and ghost tabby stripes are normal. All solid cats are ‘black on black’ and the difference can often be seen.

      As for tabbies, if the mottled pattern on the agouti hairs as they overlap can produce any number of apparent colors. A grey tabby avoids having the undercolor be orange so the effect is different to the eye.

      Like

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