The Sphynx cat (pronounced SFINGKS, /ˈsfɪŋks/) also known as the Canadian Sphynx, is a breed of cat known for its lack of fur. Hairlessness in cats is a naturally occurring genetic mutation, and the Sphynx was developed through selective breeding of these animals, starting in the 1960s.
What do Sphynx cats feel like?
Sphynx cats are as colorful as their furry counterparts, with coats that resemble peaches, fuzzy down, or chamois. They occasionally might have a little bit more hair on the tips of their ears or nose, as well as a little puff at the end of their tail. Sphynx cats are frequently compared to heated hot water bottles with suede coverings!
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Why are Sphynx cats hairless?
“It’s due to a mutation in the gene that is responsible for providing hairs with their keratin protein as they emerge from the follicle,” said Charlotte Corney, zookeeper and founder of TheWildheartTrust. “The hair is formed, but it has a weaker structure and becomes easily damaged and dislodged.”
Since their first known sighting in Toronto in 1966, when a domestic cat gave birth to a hairless kitten that was later determined to be the product of a spontaneous genetic mutation, sphynx cats were initially known as the Canadian Hairless. The first hairless cat breeding program was started by the cat, appropriately named “Prune.” Though it’s unclear if Prune or other cats with this genetic mutation are the ancestors of all contemporary hairless cats,
Although cats can naturally carry this genetic mutation, the Sphynx breed was created in the 1960s through selective breeding for this characteristic. While some Sphynx cats have short, downy fur all over their bodies or in specific places, others are completely bald, according to Corney
The recessive mutation specifically affects the keratin 71 gene (KRT71), which is essential for the development of hair. It belongs to a family of type II keratins found in all mammalian epithelial cells, which line the body’s surfaces and function as a kind of protective barrier. A protein that is expressed in the hair follicle’s inner root sheath is encoded by KRT71.
In biology, a gene is essentially turned on when it is expressed. The body produces proteins that are coded for by the DNA when instructions in the DNA are translated into the structures that are present and function in the cell. Clever.
Other phenotypes (a set of characteristics or traits of an organism) have been recorded as a result of mutations in KRT71. Previous studies have found that this gene is also responsible for curly/wavy phenotypes in dogs, mice, and rats.
Using the genomic DNA of 24 cats (Supplementary Table 2), including three hairless breeds, seven rexoid breeds, and a domestic shorthair breed as a control, all nine exons of KRT71 were amplified by PCR. For the gene KRT71, publicly available sequences from a variety of species were aligned, including Canis familiaris (XM_854730), Homo sapiens ({“type”:”entrez-nucleotide”,”attrs”:{“text”:”NM_033448″,”term_id”:”1653961749″}}NM_033448), and The partial sequence for the domestic cat, Felis catus (ENSFCAT00000000287), and Mus musculus ({“type”:”entrez-nucleotide”,”attrs”:{“text”:”NM_019956″,”term_id”:”9910293″}}NM_019956) are used to determine the exons. F. catus KRT71 can be found on GeneScaffold_3321: 736,457–745. 383. Primers (Operon, Huntsville, AL) were designed using Primer3plus (http://www. bioinformatics. nl/cgi-bin/primer3plus/primer3plus. when feasible, cgi) in the intronic regions, flanking each identified exon Using a DNA Engine Gradient Cycler (MJ Research, GMI, Ramsey, MN), primers were examined for effective product amplification. Supplementary Table 3 displays the final magnesium, temperature, and amplicon size for each primer pair. The conditions for PCR and thermocycling were as previously mentioned (Bighignoli et al. 2007). Following the manufacturer’s instructions, the ExoSap (USB, Cleveland, OH) enzyme was used to purify the PCR products of the proper lengths. Using the BigDye Terminator Sequencing Kit v3, purified genomic products were directly sequenced in both directions. Using an ABI 3730 DNA analyzer (Applied Biosystems, Carlsbad, CA), the sample was electrophoretically separated after being purified using Illustra Sephadex G-50 (GE Healthcare, Piscataway, NJ) in accordance with the manufacturer’s instructions. Sequencher version 4 software was used to confirm and align the sequences. 8 (Gene Codes Corp. , Ann Arbor, MI) and edited with BioEdit version 7. 0. 9. 0 (Hall 1999).
In the Sphynx cats, a guanine-to-adenine base substitution was seen at position 1 in intron 4. 816+1G>A). At the 5′ splice site of the intron, the guanine is a highly conserved position (Hastings and Krainer 2001; Ladd and Cooper 2002). According to a comparison of the cDNA and KRT71 genomic sequences, the GT dinucleotide sequence is located 44 bp downstream of the original splice site, r[816 1_816 43ins; 816 1g]. ). Consequently, in the altered exon 4, a different splice site is identified at base pair 44 (Fig ). This modification results in a stop codon at the insertion’s position 27, truncating KRT71 (Supplementary Fig. 1). The majority of the α-helical rod domain, which is crucial in creating heteropolymers of particular type I and type II cytokeratin through interactions between these domains, is removed from the shortened protein (Hatzfeld and Weber 1990). Combining sequence changes in exon 7 with a shortened protein that affects the α-helical rod domain may also have an impact on receptor binding, cellular targeting, the correct folding of the protein after translation, and the formation of heteropolymers of particular type I and type II cytokeratins.
A control cat, a Sphynx, and a Devon Rex’s skin samples were given by the Dermatological Service at the UC Davis School of Veterinary Medicine. RNA was isolated from the tissues using the PureLink RNA mini Kit (Invitrogen, Carlsbad, CA) after the tissues were preserved in RNAlater (Qiagen). Supplementary Table 3 shows how complementary DNA templates were created by reverse transcribed 1 μg of skin mRNA using the KRT71-5RcDNA primer to obtain exons 1–5 in the Sphynx, 1 μg of skin mRNA using the KRT71-8RcDNA primer to obtain exons 1–8 in the Devon Rex, and 1 μg of skin mRNA from hair bulbs of the control cat using the polydT primer to obtain exons 8 and 9 and the 3′ UTR of KRT71. The primers GeneRacer3R (Invitrogen) and KRT71-8FcDNA for the hair sample and KRT71-ex5RcDNA, KRT71-ex8RcDNA, and KRT71-ex1FcDNA for the skin samples were used to create PCR products in accordance with the manufacturer’s instructions (Supplementary Table 3). Thermocycle conditions were conducted as previously described (Bighignoli et al. 2007). To sequence the cats used for the KRT71 genomic analysis, genomic primers were created in the 3′ UTR region (Supplementary Table 3).
Starting at the 5′ end of intron 6 and involving exon 7, a second potentially causative polymorphism consisted of an 81-bp deletion followed by two insertions of 8 and 1 bp. A PCR reaction was conducted with the KTR71-ex7F2 and KRT71-ex7R2 primers (Supplementary Table 3) to confirm the genotype of 189 cats, comprising of wire, rexoid, and hairless breeds (Table ) as well as cats bred at random. The mutant allele was predicted to be 485 bp in size and the wild-type allele to be 557 bp. The genotype could be visually predicted based on the variation in the amplicon’s length following a run on a 2% agarose gel.
Crosses with Devon Rex were made in the early stages of the development of the hairless Sphynx breed (Robinson 1973). Of the 34 Sphynx, 26 were homozygous for the intronic SNP and 8 were heterozygous for the mutation, according to the analysis. As a result, the hr allele at the H (hairless) locus has this SNP as one of its causes. Compound heterozygotes for both the SNP and the Devon Rex-associated deletion, six Sphynx are heterozygous. These results corroborate the phenotypic and segregation analyses that were previously published (Robinson 1973) by indicating that the Sphynx allele is dominant over the Devon Rex allele, both of which are recessive to the wild type. Nevertheless, it appears that these cats have additional epistatic mutations or that hairlessness is dominant with variable penetrance in expression because two Sphynx were neither homozygous for the hr mutation nor compound heterozygous for the re mutation.
FAQ
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