Did you know that the AGA has a long history of publishing about cats? Not just the beloved felines that have commandeered many homes and communities (not to mention ecologically devastating many areas…), but also their wild brethren. In fact, Darwin even mentioned cats in his Origin of Species, where he discussed the relationships between both blue eyes and deafness as well as calico coloration and sex. In the next few blog posts I am going to describe some of the work published about our feline friends in the Journal of Heredity. A reminder to all our members, you get free access to the articles mentioned from your membership homepage on the website!
This week’s post is a bit of a mixed bag from the 1940s. We have a report on the anatomy of deaf cats that suggests genetic study, an alert(?) about the injustice of tailless cats, and investigations into Burmese and polydactyl kitties. Enjoy!
Three Generations of Deaf White Cats
Since the 1700s, deafness was a trait associated with a lack of pigmentation in cats and dogs alike. Prior study of various cats and dogs showed evidence of ear drum abnormalities as well as profound changes in the brain and inner ear. There also appeared to be a high incidence of deaf animals who also lacked pigment also having vision abnormalities.
The author of this article, Dorothy Wolff (1895-1980), pioneered a lot of work in animal models relating to otology. The rest of the article describes the microscopic anatomy of the cochlea of deaf (left side of the figure) and normal (right side of the figure) cats. She presented three generations of deaf cats, each either completely missing the organ of Corti (aka the spiral organ, this is the part of the inner ear that converts vibration into nerve impulses that are perceived as sound) or with severe pathological changes.
Her observations were “…presented with the hope that students of heredity may here find a fertile field of experimentation.” Stay tuned to see what becomes of her recommendation!
Manx Genetic Injustice
The note is short (and no author is identified), so I will just post it in entirety:
The New York Times Book Review Section records a notorious instance of genetic maldistribution. It is incorporated in a ditty popular at the Training School of the British Marines, who devil-dog like, are out to set this wrong right:
Are you are that the cats have got no
Tails in the Isle of Man?
All the other cats have tails,
In England, Ireland, Scotland, Wales.
It seems a gross injustice.
To right it is our plan.
Are you are that the cats have got no
Tails in the Isle of Man?
I am not sure what book the author is referring to, but it is quite true that a great many cats on the Isle of Man (where the Manx breed originates) experienced various levels of taillessness due to a dominant mutation and limited gene pool.
Genetics of the Burmese Cat
In 1930, a cat from Burma (Myanmar) was imported by one of the authors. At first thought to be an “off-color” Siamese (which we mentioned in an earlier post), the Burmese was a smoky brown color with darker points and topaz-colored eyes instead of a cream with points and blue eyes. It was later noted that when a Burmese was mated with a Siamese an intermediate phenotype could be produced, where the kitten was not a bright cream like the Siamese or a smoky brown like the Burmese, but an intermediate shade of tan (sounds like a classic case of incomplete dominance; see below). Thus the Burmese type was classified as “dark” (i.e. homozygous) or “light” (i.e. heterozygous).
After more crossing by curious breeders, it was determined that the Burmese gene must be autosomal (given the relatively equal numbers of male & female offspring with the trait). The authors thought that the Burmese may be an intermediate form between Siamese and silver/smoke. Therefore, there were several hypotheses:
- When Burmese is crossed to normal intensity all of the offspring will exhibit normal intensity of pigmentation.
- When purebred Burmese is mated to Siamese, all the kittens should be Burmese.
- All Siamese segregates from crosses involving Burmese should breed true for Siamese.
- When Burmese (whether purebred, or hybrid for Siamese) is mated to silver or smoke, the offspring should all be silver or smoke rather than tabby or black, as is the case when animals bearing two Mendelian coat colors due to genes at independent loci are involved.
When crossed with normal cats, the dark Burmese phenotype did not breed true, as predicted in (1). When a “dark” Burmese was mated with a Siamese, the offspring were all the intermediate shade of “light” Burmese, supporting hypothesis (2). The authors did not know of any cases where Siamese offspring from Burmese crosses spontaneously produced a Burmese, thus satisfying the prediction of (3). Interestingly, the breeders could not successfully mate a homozygous Burmese and homozygous silver/smoke, instead having to result to a homozygous silver/smoke and a heterozygous Siamese/Burmese. All offspring of this mating were silver/smoke, satisfying prediction (4).
Note: we are not done with silver & siamese cats! In fact, there is a pretty important paper about the silver gene in 1980…..
Heredity of Polydactyly in the Cat
Who doesn’t love a many-toed cat? While some breeds, like the Maine Coon, are known to have many instances of extra toes, this is a trait that exists in domestic cats as well. While cats generally only have 18 digits (5 on the front paws and 4 on the back), in cases of polydactyly they can have as many as 10 extra toes. The extra toes generally have all their “parts” such as the friction pads (aka toe beans) and claws, but are occasionally deformed. Up until this article was published (1947) it was generally thought that polydactyly was a dominant trait, but the author, C.H. Danforth, decided to put some data to this supposition.
The author established a line of polydactyl cats using two females from the Sacramento area of California, USA. Using these cats along with data from friends with extra-toed felines, Danforth established that while no normal-toed cats produced polydactyls, if one parent was polydactyl then a few kittens from the litter would also have extra toes. The affected cats had a range from an extra phalanx in a single toe creating the “thumb” look to individuals with three extra digits (see figure). The extra toes were often found only in the front paws, but in some cases the back paws also had more digits. There were no cases where the back paws had extra toes while the fronts did not.
As it seemed some of the cats in the study colony were likely homozygous, it was determined that the polydactyl gene (denoted “P” in this study) was not deleterious in its homozygous form. Danforth also hypothesizes that “P” must affect the developmental during the time of digit organization. Honestly, Danforth best sums up his conclusions:
“The evidence thus far accumulated indicates that in the cat polydactyly is conditioned by a single dominant gene whose probable chief effect is to incite some changes in the preaxial part of the limb bud causing an excess of growth in that region. From this excess tissue. enlarged or supernumerary digits are developed, none of which in itself has any genetic individuality. The trait is not related to sex. and no evidence is found that its gene is lethal when homozygous.”
We now know that polydactyly can be caused by zone of polarizing activity mutations in the sonic hedgehog gene in cats, mice, and humans (Lettice et al., 2003 & Lettice et al., 2007), although the mutation itself does not appear to explain all the variation in the effects seen in cats in particular (see Lange, Nemeschkal, & Müller, 2013). I’d say that Danforth’s hypothesis was pretty spot-on! (Side note, Superthumb Kitten sounds like an excellent band name if you ask me…)
Laura A. Lettice, Simon J.H. Heaney, Lorna A. Purdie, Li Li, Philippe de Beer, Ben A. Oostra, Debbie Goode, Greg Elgar, Robert E. Hill, Esther de Graaff, A long-range Shh enhancer regulates expression in the developing limb and fin and is associated with preaxial polydactyly, Human Molecular Genetics, Volume 12, Issue 14, 15 July 2003, Pages 1725–1735, https://doi.org/10.1093/hmg/ddg180
Laura A. Lettice, Alison E. Hill, Paul S. Devenney, Robert E. Hill, Point mutations in a distant sonic hedgehog cis-regulator generate a variable regulatory output responsible for preaxial polydactyly, Human Molecular Genetics, Volume 17, Issue 7, 1 April 2008, Pages 978–985, https://doi.org/10.1093/hmg/ddm370
Lange, A., Nemeschkal, H.L. & Müller, G.B. Biased Polyphenism in Polydactylous Cats Carrying a Single Point Mutation: The Hemingway Model for Digit Novelty. Evol Biol 41, 262–275 (2014). https://doi.org/10.1007/s11692-013-9267-y
About the Author
Miranda Wade
received her B.S. in Biological Science from Colorado State University and her dual PhD in Integrative Biology and Ecology, Evolutionary Biology, and Behavior from Michigan State University. During her time in the Meek Lab at MSU, her work consisted of using ‘omics to address various conservation questions about land-use change and microplastics exposure. She is currently the Social Media Editor for the American Genetic Association and a PostDoc in the Sin Lab at the University of Hong Kong. For her postdoctoral work, she is exploring the genomic basis of coloration in birds. She is the proud owner/caretaker of three cats.