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A rex rabbit

The rex mutation is a genetic variation in mammals that results in soft curly fur. These effects are due to changes in the structure of groups of hairs and cross-section of individual hairs. The rexed coats are unusual but occur (and have been preserved) in cats, rats, rabbits, horses, and dogs. The mutations, infrequent and spontaneous, occur in a variety of genes and genetic regulatory structures. The diversity of genetic factors results in variable coat thickness/density and fur length. A similar mutation can affect the feathers of birds.

Birds

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There are several varieties of curly-feathered domesticated birds:

Cats

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A rex cat

There are four main internationally recognised rex cat breeds: Cornish Rex, Devon Rex, LaPerm, and Selkirk Rex. Rex breeds are sometimes nicknamed "poodle cats" or "poodlecats",[4] after the curly-coat dog breed group.

There are also a number of rarer, less well known or developing rex-coated breeds, including the German Rex, Ural Rex, Tennessee Rex, Tasman Rex group,[5] and Skookum. Spontaneous rexed variants have also been observed in breeds such as the Maine Coon and Persian as well as in random-bred cats such as Ohio Rex, Oregon Rex, and California Rex, however there has been no significant attempt to develop or seek recognition for these varieties and most have died out. The Tennessee Rex is a natural-mutation breed of cat dating back to 2004, discovered by Franklin Whittenburg.[6]

Rex breeds vary considerably in appearance, from the elegant slender build of the Cornish Rex to the larger, cobby and heavy-boned Selkirk Rex. Each results from a separate mutation rather than being bred from a common ancestor. Each mutation causes the hair follicles to be oval in shape, instead of the normal regular round form, which results in hairs curling round as they grow instead of growing straight. Many of the other spontaneously occurring rex mutations have occurred and some have proven to be the same gene as the main four breeds. Some of those mutations, such as the Dutch Rex, were found to have unmanageable or unattractive fur and were not pursued as breeds.

The name rex was taken from the rabbit fancy because the first rex cat breed to be developed, the Cornish Rex, has a coat similar to that of a rex rabbit, in that it comprises only the undercoat with no topcoat or guard hairs.

Named mutations

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  • 1930s: Karakul Cat. Occurred in the US and was recorded as a novelty, but not developed as a breed.
  • 1930s: Prussian Rex. Discovered in Königsberg in what was East Prussia in the early 1930s. This rex-coated brown tomcat was named "(Kater) Munk" and has been linked to the later German Rex as he was allowed to mate freely with local cats until his death 1944. His offspring were not recorded.
  • 1944: Ohio Rex. First occurrence of rex-coated cat in Ohio, US
  • 1950s: Buckfast Blue (Buckfast Rex). Locally occurring variety in Devon, England, feral forerunner of Devon Rex
  • 1946 and 1951: German Rex. Rexed cats occurred on several occasions in different parts of Germany and some have been anecdotally linked to Kater Munk. They arose in Berlin, Essen and Sieburg, but it was the Berlin strain that gave rise to the modern German Rex.
  • 1950: Cornish Rex. The British/European style of cat is sufficiently different from the breed in North America that the latter is also referred to as "American Cornish Rex" to differentiate it and to accommodate the different breed standards.
  • 1950: Italian Rex. Three rex-coated kittens were born to a straight-haired female, but these were not pursued as a breed.
  • 1953: Ohio Rex. Second occurrence of rex-coated cat in Ohio, US. At least 4 such cats were born, but this variety lasted only 10 years with no serious attempt at creating a breed.
  • 1959: Oregon Rex. A wavy-coated bicolour female kitten was born to a straight-haired mother and named "Kinky Marcel". Test-matings with proved it to be a recessive mutation incompatible with the Cornish Rex or Devon Rexes so it was not pursued as a breed.
  • 1959: California Rex (Marcel Cat). A rex-coated tortoiseshell female called "Mystery Lady of Rodell" and her rex-coated red tabby son were bred together and resulted in further curly-furred semi-longhair cats. Test-mating found this to be compatible with the Cornish Rex so the Marcel Cat was used to expand the gene pool of Cornish Rexes in the US.
  • 1960: Devon Rex Curly-furred cats had existed in the area for a number of years and were known locally as "Buckfast Blue" because of their grey fur. These predecessors of the Devon Rex are also retrospectively referred to as "Buckfast Rex".
  • 1968–9 and 1985: Dutch Rex. The first occurrence was in Zaandam in 1968 or 1969 when a female cat produced a rexed daughter. The daughter produced rexed offspring when mated to unrelated straight-haired males, including Siamese cats, demonstrating this to be a dominant mutation. The fur tended to form dreadlocks and had a coarse, unruly texture. The cats were also prone to balding. Cat fanciers believed the strain originated from an American Wirehair belonging to military personnel. The mutation reappeared in 1985 and was also known as the Wirehair Rex. These cats were traceable as descendants of the discontinued Dutch Rex breeding program. The last known Dutch Rex was a female cat of unknown origin found in Amsterdam in the late 1990s. The dominant mutation produced a rex type of coat in the heterozygote and a sparse coat in the homozygote.
  • 1972: Victoria Rex. A curly-furred cat named Tuoh was found in the Victoria area of London. The fur was different from the Devon Rex and the cat was to have been test-mated to a Cornish Rex. The outcome of test-matings appears not to have been recorded.
  • 1979: Sieburg Rex. A spontaneously occurring rex-coated bicolour male cat originally named Pushkin, and later renamed Kater Preu, was used in the German Rex breeding programme. He turned out to have a different mutation to the Berlin cats, and produced straight-haired offspring when mated to them, so he was neutered.
  • 1982: LaPerm
  • 1987: Selkirk Rex
  • 1988 and 2002: Maine Waves/Rexed Maine Coon. Originally occurred in British breeding lines in the 1980s and caused controversy as the GCCF rules do not allow for spontaneous mutations to be registered as separate breeds. Test matings with Devon Rexes and Cornish Rexes were inconclusive. Test-matings indicated that the mutation was either recessive or incomplete dominant gene and did not result from mis-mating of a Maine Coon to either of those breeds. Accusations of mis-mating and unhealthy cats persisted. In the 1990s, Rexed Maine Coons (and carriers of the mutation) were neutered to avoid spreading the unwanted gene. In 2002, several Rexed Maine Coons were born in New York, US. Although blamed on the effects of the 9/11 attack, it was more likely due to the rex mutation being in the gene pool.
  • 1990s: Dakota Rex. There were plans to establish this as a breed.
  • 1990s: Missouri Rex. The mutation was found to be different from the Devon Rex and Cornish Rex mutations and it was planned to establish this asa breed. Financial problems led to most of the cats being euthanized.
  • 1991: Urals Rex. Although not recognised until 1991 by the emerging cat fancy in Russia after glasnost, the Urals Rex had been reported in and around Yekaterinburg since the Second World War. There were two breeding populations carrying the same mutation which was known to be different from the German/Cornish Rex rex mutation. By 1991 the cats were greatly inbred and work was needed to expand the gene pool.
  • 1994: Bohemia Rex/Czech Curly Cat. Although not recognised until 1994, this longhair rex of Persian conformation has existed in Liberec, The Czech Republic since 1981. It arose when curly kittens were born in a pedigree Persian litters. The parents were traced back to two blue Persian males imported from Germany in the 1970s. These males may have inherited a spontaneous mutation or may have carried the German Rex mutation due to Persian cats being used in the German Rex breeding program and some of the straight-coated offspring being registered as Persians. Test-matings found that only some Bohemia Rexes have the Cornish (German) Rex mutation and that there is an unknown second rex-causing gene involved. There was little interest in this variety until after the recognition of the Selkirk Rex Longhair.
  • 1994: Poodle Cat (Pudelkatze). A German variety, now possibly extinct due to German legislation, developed from the Scottish Folds and Devon Rexes
  • 1998: Skookum (previously LaMerm). A breed developed in the US. from LaPerms and Munchkins
  • 1998 and 2003: Tasman Manx (also nicknamed Manx Rex). A spontaneously occurring rex-coated Manx cat. This arose spontaneously in pedigree Manx lines in Australia and New Zealand, not from crossbreeding. Test-matings to Devon Rex produced only straight-haired kittens. The fur also appears different from the Cornish Rex mutation, but test-matings are required. Curly-furred Manx cats were all traceable to an outcross mating (to widen the Manx gene pool) in Australia which used a cream Persian male from European bloodlines. It is suggested that these may, therefore, be related to some Bohemia Rex cats.
  • 1998: Australian Rex. Arose in 1998, but not reported until 2005. Cats with coats similar to Cornish Rexes occurred in non-pedigree litters in an area where there were no known Cornish Rex cats. The cats were small and litter sizes were typically 1 or 2 kittens. Breeding was not controlled and many of the cats disappeared or were neutered, leaving only one breeding male. Cat breeding is not encouraged in Australia and this variety may now be extinct.
  • 2001: Iowa Rex. A male cat sired curly-coated kittens, including dreadlocked longhairs, in several litters. The Iowa cats were large and muscular with notably broad muzzles. Their discoverer was seeking an experienced breeder to take these on as a developing breed.
  • 2001: Ruffle. This combined the American Curl's ear type with the Cornish Rex fur type, but was not further developed under this name. There are differing accounts as to whether it occurred spontaneously or through deliberating crossbreeding.
  • 2003: Brooklyn Wooley. Several "Wirehair Rexes" were born in Brooklyn, New York, US, but did not survive. Subsequent litters born to the same parents survived and are being developed into a new breed. Kittens may be born partly bald or go through a bald phase before developing the curly coat. It was initially thought to be identical to the short-haired LaPerm, but was later found to be a new recessive mutation.
  • 2003: Prairie Rex. Rexed cats were found at a farm in Saskatoon, Canada and had been breeding freely for around 10 years. Several cats were taken on by a breeder, but were badly inbred resulting in poor health. They were traceable to a chocolate point rexed male and the line appears to have died out. The last of the line were neutered due to their poor health.
  • 2003: Hoosier Rex. A curly-haired female and 4 curly-haired kittens were found in Indianapolis and given to an animal shelter where they were all neutered. The animal shelter had received similar cats over the previous two years. The mutation cannot be researched due to a legally binding neutering rule.
  • 2004: Tennessee Rex (T-Rex). Two curly-coated were taken in by a Chattanooga cat-lover who was sufficiently impressed by their appearance to pursue this as a new breed. In addition to their curly fur, many of the cats had a "satin" or "glitter" mutation resulting in glittering fur.
  • 2009: Helki. Developed in California from South Sacramento feral cats with a semi-rexed coat. The silky or fleecy coat contains a mix of straight and wavy guard hairs and it appears to be a dominant mutation. the name means "touch" in the Miwok language.
  • 2015: Australian Satin. Kim Gale discovered a litter of 4 rex satin domestic cats in Queensland Australia. The breed is being Pursued By Kim Gale, the Hair is silky with a sparkle, so far looks best on red, but other colours are being explored. Genetically it is a recessive mutation.

Dogs

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Horse

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Closeup of American Bashkir Curly horse coat in winter

Pig

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Rabbits

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See also: Domestic rabbit § Genetics

A great variety exists within rex rabbits. They vary from very dense and short-haired varieties (Standard Rex) to long-and-curly-haired breeds (Astrex).

The rex rabbit was introduced in 1919 by Abbe Gillet from a spontaneous mutation. The next rex rabbit was discovered in the hutches of a breeder in Lübeck, Germany in 1926. This breed was originally called Deutsch-Kurzhaar and is due to the r2 (dek) gene. In 1927, yet another short-hair rabbit was discovered in the hutches of the French breeder Madame Du Bary, a fancier of Himalayan (ch-) rabbits. This breed was called Normannen-Kurzhaar and is due to the r3 (nok) gene. [7]

Of the three genetic sources of rex rabbits, the one due to the gene r1 is the most popular with fanciers and has the simple Mendelian inheritance pattern of autosomal recessive. It was not linked with any other genes known at the time although it was eventually found to be in the same linkage group as r2.[8]

The phenotype of r1 and r2 is a completely normal coat but r1 or r2 alone produces a short coat with curly whiskers. Although the phenotypes are identical for each gene, the linkage distance was eventually worked out.[8] The gene r3 is independent of r1 and r2 in breeding tests so they fall on different chromosomes.[7]

The mutation associated with r1 was recently studied using modern genetic tools. A deletion of a single nucleotide was found in LIPH (lipase member H gene) of rex rabbits. In humans, this gene is associated with alopecia (hair loss phenotypes). This mutation results in a frameshift that causes the mRNA transcription machinery to sense the end of the gene prematurely. The stop codon generated by the deletion may be shortening the protein by 19 amino acids. The exact mechanism was not determined but the deletion is necessary and sufficient for the rex phenotype.[9]

Rodents

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Guinea pigs

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Hamsters

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Rex golden hamsters first appeared in the 1970s, characterised by curly whiskers and a curly coat; the curls in the coat are easily visible in short-coated hamsters but more difficult to see in long-coated ones.[10][11]

Rex in Campbell's dwarf hamsters is not recorded as to when it first appeared. Unlike with golden hamsters, the rex coat in Campbell's dwarfs is commonly very sparse and gives a bald appearance. The whiskers are curled.[11]

Mice

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Rat

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References

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Revisions and contributorsEdit on WikipediaRead on Wikipedia

Rex mutation

View on Grokipedia
from Grokipedia
The Rex mutation refers to a class of independent genetic variations observed across multiple mammalian species, including rabbits, cats, mice, rats, dogs, and livestock such as horses and pigs, that disrupt normal development and shaft formation, resulting in characteristic curly, wavy, or crimped textures. Analogous mutations affect structure in birds. These mutations typically affect the structure of guard hairs, awn hairs, and sometimes , producing a soft, coat without altering overall body size or viability. The term "Rex" originated in the early with the discovery of recessive coat mutations in domestic rabbits, where three distinct genes—designated re1, re2, and re3—were identified as causing shortened, curled guard and awn hairs while leaving underfur largely unaffected. The first mutation appeared in 1919 in , followed by others in the 1920s, leading to selective breeding for the trait in and the . Analogous mutations in other species were later classified as "Rex" due to their phenotypic similarity, facilitating comparative genetic research on hair morphogenesis. In cats, Rex mutations have been instrumental in establishing distinct breeds, each arising from spontaneous events and fixed through breeding programs. The Cornish Rex, originating in England in 1950 from a recessive mutation in the LPAR6 gene (a 4-bp deletion at c.250-253delTTTG), features tight, uniform curls across a short, dense coat and is inherited autosomally recessive. The Devon Rex, discovered in 1960 in England, results from a complex insertion-deletion in the KRT71 gene causing splicing errors and loose, wavy fur, also autosomal recessive. The German Rex, first noted in the 1930s in Prussia, shares the KRT71 locus with the Devon Rex but represents a separate variant. In contrast, the Selkirk Rex, emerging in 1987 in the United States, stems from an autosomal dominant splice-site mutation in KRT71, producing variable curls that are tighter in homozygotes. These feline Rex traits are generally benign but can interact with other coat genes, influencing breed standards and outcrossing strategies. Beyond cats and rabbits, Rex mutations have been documented in laboratory and domesticated rodents, aiding studies of epidermal differentiation. In mice, at least six Rex loci exist on various chromosomes, with the original Re mutation (discovered 1939) causing wavy vibrissae and guard hairs via altered keratin expression. Rats exhibit a dominant Rex (Re) allele leading to sparse, curled coats in heterozygotes and more severe baldness in homozygotes. Contemporary rabbit Rex breeding primarily utilizes a frameshift deletion in the LIPH gene (1362delA), which impairs essential for integrity and is autosomal recessive. Overall, Rex mutations highlight conserved genetic pathways in mammalian hair growth, with no widespread health detriments reported beyond occasional skin sensitivities in affected individuals.

Overview

Definition and characteristics

The rex is a primarily observed in mammals that results in soft, curly, or wavy fur due to alterations in the structure, which lead to anomalies in the shaft. The term "Rex" describes a resulting from various independent mutations at different genetic loci across . This mutation affects the development and arrangement of hair types, including a reduction in the number and length of guard hairs—typically the longer, coarser outer hairs—and modifications to the undercoat, resulting in a denser, more uniform curl pattern. Characteristic physical traits of the rex mutation include curly , known as vibrissae, which contribute to the distinctive tactile appearance, along with a , velvety texture that gives the a soft, rippled quality. Variations in density can occur, with some individuals exhibiting tighter curls or sparser coverage, and in some like rats, extreme homozygous cases may progress to partial or near-complete hairlessness, though this is not the primary or universal across all rex variants. The overall effect is a altered pelage that contrasts with straight-haired norms, often enhancing insulation or sensory functions through its unique morphology. Unlike other coat mutations, such as , which primarily affects pigmentation and results in solid white fur without structural changes to shape, or hairless variants like the Sphynx mutation that cause near-total absence of due to keratin deficiencies, the rex mutation specifically emphasizes curl and waviness in existing rather than elimination or color alteration. This focus on conformation distinguishes it as a rexoid centered on follicle-derived curling. Analogous effects appear in non-mammals, where similar genetic variations produce curly or frizzled feathers in birds, altering barb structure for a wavy appearance without loss of coverage.

Historical background

The rex , characterized by curly or wavy fur, first emerged as a documented in rabbits in 1919 in , where a spontaneous recessive produced a of wild gray rabbits with short, coats. This discovery, attributed to Abbé Gillet in the village of Louché-Pringé, marked the initial observation of the rex phenotype in domestic animals and led to efforts that established the breed. By 1924, the breed was showcased at the International Rabbit Show, gaining international recognition, and was imported to the in 1928, where it was officially accepted by the in 1929. In cats, rex mutations appeared independently in the mid-20th century, beginning with the in 1950 in , , when a curly-coated cream male named Kallibunker was born in a litter of barn cats owned by Nina Ennismore. This recessive mutation prompted breeding programs that formalized the breed by the late 1950s. The followed in 1960 in Devonshire, , with the birth of a curly-haired named Kirlee, discovered by Beryl Cox, leading to its recognition as a distinct breed by the Governing Council of the Cat Fancy in 1967. Earlier, the was discovered in 1951 in , , by Dr. Rose Scheuer-Karpin, who found a curly-coated stray cat named Laemmchen (born around 1946–1947); this revived interest in the breed, which gained formal recognition in Europe by the 1980s. Later developments in the 1980s introduced dominant rex variants in the United States, such as the Selkirk Rex, originating from a 1987 litter in Montana where a curly-furred kitten named Miss DePesto emerged from a stray cat, resulting in breed acceptance by The International Cat Association in 1992. Similarly, the LaPerm arose in 1982 on an Oregon farm owned by Linda Koehl, starting with a bald kitten named Curly that developed a curly coat, leading to provisional recognition by the Cat Fanciers' Association in 1996. More recently, the Tennessee Rex appeared in 2004 in Tennessee, discovered by Franklin Whittenburg among feral cats, representing an experimental breed that remains in development without full championship status as of 2025. These spontaneous mutations in rabbits and cats since the early 20th century exemplified broader patterns in domestic and wild animals, where rex variants spurred selective breeding for aesthetic and functional traits, influencing breed standards worldwide.

Genetics

Molecular mechanisms

The rex mutation primarily involves alterations in genes encoding structural proteins of the hair follicle, particularly keratins expressed in the inner root sheath (IRS). The KRT71 gene, which codes for a type II keratin crucial for IRS integrity, is frequently implicated; mutations such as splice site variants or deletions in its α-helical rod domain disrupt keratin intermediate filament assembly, leading to IRS structural instability. This instability impairs the IRS's role in guiding and straightening the emerging hair shaft, resulting in wavy or curly coats as the hair follows an irregular path through the follicle. Similar effects occur in other IRS keratins, where amino acid deletions compromise filament bundling and desmosomal anchorage, essential for maintaining follicle architecture during hair growth. Mutations in genes, such as LIPH (encoding H) and its receptor LPAR6, also contribute to rex phenotypes by altering signaling in the . LIPH produces (LPA), a mediator that regulates follicle differentiation; deletions or frameshifts, like the 1362delA variant, reduce LIPH enzymatic activity and expression in the IRS, disrupting LPA-LPAR6 signaling and leading to abnormal hair shaft curvature and reduced hair length. This pathway influences the asymmetry of follicle proliferation and dermal papilla function, promoting elliptical hair cross-sections that curl upon emergence. In contrast, mutations in desmosomal components, such as desmoplakin (DSP), weaken cell-cell adhesions in the follicle, indirectly affecting bundling and causing woolly hair textures akin to rex variants. Across taxa, mammalian rex mutations target IRS keratins for helical fur growth, reflecting conserved pathways in .

Inheritance patterns

The Rex exhibits predominantly autosomal recessive across many and breeds, requiring homozygosity at the relevant locus for phenotypic expression of the curly or wavy coat. For instance, in cats, the trait is inherited recessively, with affected individuals possessing the homozygous re/re genotype, while heterozygous carriers (Re/re) display normal straight coats and can pass the without showing symptoms. Similarly, the follows this pattern, where only homozygous rd/rd cats express the curly coat. Exceptions to this recessive pattern exist, notably in the cat, where the mutation is inherited as an autosomal dominant trait with incomplete . Heterozygous (Cu/+) cats exhibit the characteristic curly coat, while homozygous (Cu/Cu) individuals display tighter, denser curls and a more slender build, though the trait is viable in both states without reported lethality. Homozygous expression of recessive Rex mutations typically results in the full curly phenotype, but certain historical lines, such as early , carried associated lethal factors that could lead to embryonic or neonatal lethality when homozygous or in specific combinations. In contrast, dominant forms like show graded effects, with homozygotes having enhanced curliness but potential for temporary coat thinning. Combining different Rex mutations at separate loci—known as "double Rex" in cats, such as Cornish and —can produce atypical outcomes, including near-hairless phenotypes due to disruptive interactions in development, often accompanied by sensitivities or grooming-related health issues. Modern genetic testing enables identification of carriers and informs breeding decisions to avoid deleterious combinations. For example, DNA tests offered by the UC Davis Veterinary Genetics Laboratory detect Rex variants in cats, allowing breeders to screen for homozygous recessives or carriers to prevent expression of the trait or risky matings. Rex mutations do not act in isolation and can interact with polygenic factors, such as dilution genes (e.g., the dilute/dense locus) or pattern modifiers, altering coat texture, density, or color intensity in affected individuals. These interactions may enhance waviness in combination with certain alleles or lead to patchy expression, emphasizing the need for comprehensive genetic profiling in breeding programs.

In Cats

Major rex breeds

The major rex breeds in cats include the Cornish Rex, Devon Rex, Selkirk Rex, and German Rex, all developed from spontaneous mutations that produce distinctive curly or wavy coats while maintaining a generally healthy profile without major rex-specific diseases, though some lines may show predispositions like hereditary myopathy in Devon Rex cats. These breeds are recognized by major cat fancier organizations such as The Cat Fanciers' Association (CFA) and The International Cat Association (TICA), with breed standards emphasizing their unique fur textures, slender builds, and playful temperaments. The originated in 1950 in , , from a litter born to a feral barn named Serena, where one kitten, Kallibunker, exhibited a tight, curly coat resembling fur due to a recessive four-base-pair deletion in the LPAR6 gene, causing a frameshift and premature that alters structure. This slender, whip-tailed breed with large ears and a racy build was imported to the in 1957 and achieved CFA championship status in 1964, with TICA recognizing it shortly thereafter; its coat lacks guard hairs, consisting only of down and awn hairs, resulting in a soft, wavy texture that requires minimal grooming. The emerged in 1960 near Devon, , from a litter of a , featuring loose, pixie-like waves in its short, soft coat caused by a distinct recessive in the KRT71 , which disrupts filament assembly in hair shafts and leads to curly whiskers and fur. Known for its elf-like appearance with large, low-set ears, big eyes, and a stocky yet athletic body, this breed was developed through and gained CFA championship recognition in 1979, while TICA accepted it earlier; cats often exhibit high energy and affectionate behavior, though some are prone to a separate hereditary linked to a COLQ variant, manifesting as in kittens. The , discovered in 1987 in , , from a curly-coated shelter named Miss DePesto, represents the only dominant rex mutation in cats, stemming from a splice site variant in the KRT71 gene that produces a spectrum of curliness from loose waves to tight curls in a dense, plush coat available in both short and longhair varieties. This teddy bear-like breed with a rounded head, stocky build, and full cheeks was outcrossed to and British Shorthairs initially, achieving TICA advancement to championship in 1992 and CFA full recognition in 2015; its dominant inheritance allows for variable expression, with homozygous cats showing tighter curls, and it maintains robust health without unique rex-related issues. The traces its roots to the 1930s in (now ), , where a curly-coated named Kater Munk appeared in a domestic litter, later bred to establish the line with a soft, marcel-wave coat identical to the due to the same recessive LPAR6 , though early assumptions suggested a unique . This medium-sized, elegant breed with curled whiskers and a friendly disposition was recognized in Europe by the 1960s and imported to the in the , but remains rare today, with TICA granting it full championship status while CFA does not recognize it separately, often merging it with standards; health profiles are similar to other rex breeds, with no breed-defining genetic diseases.

Minor and extinct rex mutations

The represents one of the minor rex mutations in cats, characterized by a dominant curly coat gene (Lp) that produces loose to tight waves or curls in both short- and long-haired varieties. Originating from a spontaneous in a cat in in 1982, the breed was developed by Linda Koehl, who observed curly-haired kittens among straight-coated litters and confirmed the dominant inheritance pattern through . Unlike recessive rex mutations in major breeds such as the or , the LaPerm's curl is expressed in heterozygotes, allowing for broader genetic diversity but requiring careful to avoid over-curling or bald patches in homozygotes. Today, the remains recognized by organizations like (TICA) and The Cat Fanciers' Association (CFA), though it occupies a niche status due to its limited popularity and the maintenance challenges of its textured, medium-length coat, which can mat if not groomed regularly. The Tennessee Rex, another minor variant, emerged from a spontaneous recessive combining rex curling with a satin sheen in 2004, when a stray domestic shorthair in produced curly-coated kittens. This pleiotropic affects hair structure to create a glossy, wavy coat in both long- and short-haired forms, distinct from KRT71-based curls in breeds like the . Developed primarily by breeder Franklin Whittenburg, the Tennessee Rex achieved provisional recognition with TICA in 2009 and advanced to championship status as of 2025, though its rarity stems from small breeder numbers and the need for to non-rex cats to maintain health and coat quality. Unlike more established rex breeds, the Tennessee Rex's dual traits have not led to widespread adoption, positioning it as a niche rather than a major lineage. Several early rex mutations proved short-lived or extinct due to breeding challenges. The Ohio Rex, first reported in 1944 from a curly-coated kitten in , exhibited a soft, wavy coat similar to the but was not systematically bred, leading to its loss by the 1950s amid issues and poor coat viability in subsequent generations. Similarly, the Oregon Rex arose in 1959 from a litter in featuring tight curls and minimal guard hairs, initially thought to be a unique recessive ; however, due to breeding incompatibilities with established rex breeds, surviving lines were absorbed into the Cornish program rather than maintained separately, effectively extinguishing it by the 1970s. These cases highlight common pitfalls for minor rex variants, including matting-prone coats that required excessive grooming and associated skin sensitivities from altered hair follicles. Experimental crosses, such as those between Sphynx (hairless) and rex breeds like the , have produced hybrid offspring with variable curly or sparse coats, but these lack standardization and are not recognized as distinct rex . Such hybrids often display inconsistent curl patterns due to the interaction of recessive hairless (hr) and rex (re) alleles at the KRT71 locus, resulting in coats prone to health issues like skin infections from reduced protection. Efforts to develop "Sphynx Rex" lines in the early were discontinued due to unpredictable phenotypes and welfare concerns, with most absorbed into parent breeds or abandoned. Overall, minor and extinct rex underscore the fragility of novel coat genes in cats, where viability hinges on coat functionality, , and breeder commitment, often leading to absorption into major lines like the or for preservation.

In Dogs

Genetic variants

The rex coat phenotype in dogs is primarily associated with mutations in the KRT71 gene, which encodes a protein essential for hair shaft structure in the inner root sheath of hair follicles. Two distinct alleles have been identified in this gene. The first, a missense (c.451C>T, p.Arg151Trp), was reported in and causes curly or wavy coats through disruption of keratin filament assembly. This exhibits incomplete dominance: heterozygous dogs typically display wavy coats, while homozygous individuals show tighter curls. A second KRT71 , an 8-bp variant (c.1266_1273delinsACA) in 7, was identified in 2018 in unrelated curly-coated dogs across breeds such as the Barbet and . This variant causes a frameshift (p.Ser422Argfs*) and loss of the , leading to an altered and extended KRT71 protein and a curly similar to but potentially subtly distinct from the p.Arg151Trp . Like the first variant, it affects structure, analogous to a 7-bp deletion in the Krt71 that causes curly in heterozygotes and alopecia in homozygotes. Mutations in the RSPO2 gene, encoding R-spondin-2, contribute to rex-like curly coats in certain breeds by altering Wnt signaling pathways that regulate development. A dominant 167-bp insertion in the 3' (3' UTR) of RSPO2 increases , resulting in wiry or curly coats with furnishings (e.g., in the ). When combined with KRT71 variants, this insertion produces tight, curly wiry coats, as homozygous or heterozygous states for RSPO2 enhance the curl intensity from KRT71 disruptions. These rex variants differ from non-rex curly coats, such as those influenced by FGF5 , which primarily affect length rather than shaft structure or curl pattern. For instance, the standard poodle's long curly arises from KRT71 for curl combined with FGF5 for elongation, but FGF5 alone does not induce waviness or curls. gene disruptions like those in KRT71 generally impair shaft integrity, leading to the characteristic rex waviness or curl without altering overall growth cycles.

Affected breeds and traits

The is one of the primary dog breeds exhibiting rex-like traits, characterized by a dense, tight-curled single coat that provides exceptional water resistance, aiding in waterfowl retrieval. Originating in the during the 19th century, this breed's coat evolved to protect against cold water and harsh weather conditions during hunting. The displays rex-associated coat features through its medium-length, water-repellent outer layer, which ranges from loose waves to tight curls, complemented by a dense, rex-like undercoat that insulates and sheds water effectively. Developed as a versatile , this breed's coat supports its role in retrieving game from wetlands, with the wavy or marcel-patterned texture enhancing and dryness after swims. Hybrids such as the and those involving often show variable expression of rex traits, with curly or fleece-like coats that appeal to owners seeking qualities due to low production. These crosses, derived from genetics, produce soft, wavy-to-curly textures that reduce spread, though coat consistency can vary across generations. Common traits among these rex-influenced breeds include reduced shedding compared to straight-coated varieties, a soft and plush texture that traps air for insulation, and a tendency toward matting if not regularly groomed, necessitating frequent brushing to maintain . Unlike some genetic conditions, the rex in does not carry major unique risks, such as increased susceptibility to disorders beyond general grooming needs; however, homozygotes for the second KRT71 variant may be at risk for follicular dysplasia. Breeders selectively pair individuals to preserve the desired curl pattern while minimizing dilution toward straight-haired offspring, ensuring the trait's stability. The of rex coats in most breeds follows an incomplete dominant pattern: heterozygotes show wavy coats, while homozygotes exhibit fuller curly expression.

In Livestock

Horses

The rex mutation in is primarily exemplified by the breed, which features a distinctive curly resulting from a dominant genetic variant. This mutation causes the hair to form tight curls, particularly in the mane, , and body during winter, providing enhanced insulation against cold weather. The breed's origins trace back to the mid-20th century , with the first documented curly born in 1957 in to straight-haired parents, marking a spontaneous appearance of the trait. Subsequent breeding efforts in the led to formal recognition by registries, though the name "Bashkir" was later deemed misleading as the is not linked to Russian Bashkir horses but rather to occasional curly individuals in American stock of diverse ancestry. The curly coat sheds extensively in summer, often leaving with a smooth or nearly bald appearance, which aids in heat dissipation. Genetically, the curly follows an autosomal dominant pattern, with curly foals possible from one curly and a straight-haired mate. Research has identified causative variants in the KRT25 gene (encoding keratin 25) and the SP6 gene (a ), where an epistatic interaction between them produces the curliness; horses homozygous for the KRT25 variant often exhibit additional hypotrichosis (reduced hair). A similar curly phenotype is also observed in the Foxtrotter , arising from the same epistatic interaction between KRT25 and SP6 variants. American Bashkir Curlies are valued for their qualities, attributed to lower and altered proteins, though scientific studies show mixed results on reduction. They demonstrate strong cold resistance due to the insulating winter but may have more sensitive requiring careful management. These horses excel in and other versatile disciplines, owing to their hardy constitution and friendly . The does not introduce breed-specific issues beyond general equine concerns, but the curly demands intensive grooming to prevent matting and skin irritation during shedding seasons.

Pigs

The , also known as Mangalitza, is a Hungarian breed renowned for its distinctive curly, woolly , representing a rex-like in swine. Developed in the mid-19th century through crosses between local Serbian Sumadia pigs and Hungarian breeds, possibly with influences from , the became a prominent lard-type in the , valued for its fatty and adaptability to outdoor farming. The breed's thick, ringlet-formed hair provides excellent insulation, enhancing cold tolerance and allowing Mangalica pigs to thrive in harsh winter conditions without extensive , a trait that supports sustainable, low-input . This curly coat contributes to superior fat marbling and high overall carcass fat content (65-70%), with levels higher than in commercial breeds (typically 3-10%, up to 18% in some muscles), resulting in tender, flavorful ideal for production, such as and , where the remains stable during curing. Genetically, the curly hair in pigs follows an autosomal dominant pattern, as confirmed by matings with straight-coated breeds where all F1 offspring exhibited curly coats. Genome-wide studies have identified selection signatures in (KRT) and keratin-associated protein (KRTAP) gene clusters, alongside variants in CYP4F3 and TRPM2 genes that co-segregate with the trait, suggesting roles in development and ; however, a direct homolog to the KRT71 seen in feline rex breeds remains unconfirmed. Following , the nearly went extinct due to the rise of lean commercial breeds and , with only a few dozen individuals remaining by the 1990s; conservation efforts by Hungarian breeders and international enthusiasts have since revived the population for heritage farming and gourmet markets, emphasizing its economic value in specialty production. While rare instances of curly coats occur in wild boars, these have not been domesticated or selectively bred like the .

Rabbits

The Rex mutation in rabbits produces a distinctive short, velvety due to a recessive genetic alteration affecting structure. This mutation was first identified in in 1919, arising spontaneously in a of wild gray rabbits, where one kit exhibited an unusually , uniform length without longer guard hairs. The resulting Standard Rex features dense, soft that lies close to the body, making it prized for its aesthetic and tactile qualities. The standard Rex coat is governed by the recessive re allele (also denoted as r1), which equalizes the length of undercoat and guard hairs, creating a plush texture. In homozygous form (re/re), this leads to the characteristic velvety appearance, while heterozygous rabbits (Re/re) display normal fur. The re locus is linked to another Rex variant (r2), but the primary mutation responsible for the Standard Rex phenotype is a single deletion in 9 of the LIPH gene (1362delA), confirmed in 2011. This deletion causes a frameshift, introducing a premature that disrupts H function, leading to defects in hair follicles and altered shaft formation. A related variant, Astrex (often described as a "double Rex" due to compound effects), occurs in rabbits homozygous for both the re allele and an additional recessive wavy gene (wa/wa), typically on a Rex background. This combination produces an ultra-short, wavy, coat with curled , giving a curly or lamb-like appearance, though the fur remains fragile and prone to matting. Astrex coats are rare and unstable, often molting irregularly, and are associated with underlying concerns that limit breeding viability. Rex rabbits are represented in breeds such as the Standard Rex, with color varieties including Castor Rex, which features a rich, agouti-like pattern resembling pelt. Early developments also incorporated Rex traits into lines like for fur quality enhancement. Commercially, Rex rabbits are valued for balanced meat and production, with their dense pelts used in the garment industry for soft, durable linings; the shorter guard hairs reduce , making the fur somewhat less allergenic compared to standard rabbit coats. Overall, Rex rabbits exhibit good health and reproductive viability under standard conditions, with litters averaging 6-8 and no major inherent defects in the standard form. However, Astrex variants may experience reduced and increased susceptibility to skin issues due to the compounded genetic effects, advising against for this trait.

In Rodents

Guinea pigs

Two independent recessive Rex mutations (designated re and re-2) in guinea pigs first emerged in the late 1970s in the , originating from of Dutch guinea pigs and gaining recognition as a distinct type by the early 1980s. These autosomal recessive traits produce a distinctive curly with rosette patterns and kinked , altering the typical smooth pelage to an upright, wavy appearance. The mutations affect development, resulting in short, dense fur that lacks prominent guard hairs and stands on end, giving the animal a , hedgehog-like look. Phenotypically, Rex guinea pigs exhibit soft, wavy hair shafts with no straight segments. While the molecular basis is not yet characterized, the phenotype is analogous to disruptions in inner root sheath integrity seen in Rex mutations of other mammals. While the coat is generally soft and even, the curls can lead to health concerns, including trichiasis where facial hairs irritate the eyes, potentially causing corneal ulcers or infections if untreated. Owners should monitor for eye discharge or squinting and consult a veterinarian for trimming or lubrication as needed. In terms of varieties, the American Rex represents the standard form recognized by the American Cavy Breeders Association, featuring the classic wiry texture, while the variety is genetically distinct—recessive on a different locus—and produces a similar but softer, bouncier coat more prevalent . Rex guinea pigs are highly popular in the pet trade due to their calm, sociable and low-maintenance short coats, though breeding requires careful pairing of homozygous recessives to maintain the trait. Regular grooming, including weekly brushing, is essential to prevent matting around the hindquarters and face, especially in humid environments.

Hamsters

The rex in hamsters primarily affects Syrian (Mesocricetus auratus) and Campbell's dwarf (Phodopus campbelli) varieties, resulting in a curly or wavy texture due to alterations in structure. In Syrian hamsters, the first appeared in 1970 and was formally reported in 1973 as a novel autosomal recessive trait. It produces a short, soft, plush-like with curly vibrissae () and reduces body weight by approximately 14% at 21 days of age, though it has no impact on viability or fecundity. The genetic basis involves a in the Krt71 , which encodes a protein essential for inner root sheath integrity in follicles. In Campbell's dwarf hamsters, the rex mutation manifests as curly whiskers and a similar plush, lifted coat texture, also inherited recessively, though the specific genetic variant remains less characterized than in Syrians. This coat type emerged in the late 1990s in the UK, contributing to one of four recognized coat variations (normal, satin, wavy, and rex) in the breed. The softer fur compared to wild-type hamsters enhances their appeal as pets, but the curly structure can lead to occasional matting, necessitating gentle brushing for maintenance. Both Syrian and Campbell's rex hamsters originated from laboratory breeding programs—Syrians from early 20th-century research in the Middle East and dwarfs from Soviet collections in the 1960s—before becoming established in the pet trade. Today, rex variants are recognized standards in hamster fancy organizations, valued for their distinctive appearance without compromising health.

Mice

In laboratory mice, multiple genetic variants produce rex-like phenotypes characterized by altered hair structure, with the primary loci including the Re (rex) locus on chromosome 11 and the frizzy (fr) locus on chromosome 7. The Re locus, associated with genes such as Krt25 and Krt27, is dominant and results in curly vibrissae (whiskers) and short, wavy guard hairs that are irregularly distributed across the coat, leading to a reduced overall fur length and texture. In contrast, the fr mutation on chromosome 7 is recessive, producing wavy or curly vibrissae from birth and a plush, wavy pelage in homozygotes (fr/fr), though it does not significantly shorten hair length. These phenotypes arise from disruptions in keratin intermediate filament assembly within the hair follicle's inner root sheath, as confirmed by studies on targeted mutations and knockouts of associated keratin genes like Krt25 and Krt27. For instance, mutations in the helix termination motif of these type I inner root sheath keratins impair filament bundling, causing irregular hair shaft diameters and the characteristic waviness. While most rex variants in mice are viable in both heterozygous and homozygous states, certain alleles at related loci, such as those linked to Gsdma3 on , can lead to more severe outcomes like progressive alopecia in homozygotes, though not outright lethality. Rex mutant mice have served as key models for studying biology and disorders since the mid-20th century, with significant research in the 1990s focusing on their utility in elucidating follicle cycling and differentiation. These strains, particularly those with Re or Rewc alleles, exhibit altered hair growth phases, providing insights into the molecular mechanisms of hair shaft formation and potential parallels to human ectodermal dysplasias. models of Krt25 and Krt27 have further validated these roles by recapitulating the curly whisker and wavy coat phenotypes, emphasizing the genes' importance in maintaining hair integrity. Beyond research, rex variants are selectively bred in strains for pet and show purposes, where the curly coat enhances aesthetic appeal in varieties like self black or longhaired crosses, distinguishing them from wild-type with straight fur. These domesticated lines maintain the recessive or dominant rex traits through careful breeding, avoiding wild-derived populations to preserve the exhibition-quality waviness.

Rats

The Rex mutation in rats (Rattus norvegicus) is an autosomal semi-dominant genetic variant symbolized as Re, first developed in by geneticist Roy Robinson in 1976 and standardized as a variety by the National Fancy Rat Society the same year. This mutation, located on , results in distinctive coat alterations without significant health impairments in heterozygous individuals, making it a valued trait in both pet breeding and research. Heterozygous rats (Re/re) display a curly or wavy pelage with shorter, harsher guard hairs and bent vibrissae, while homozygous rats (Re/Re), often termed "double Rex," exhibit more pronounced effects including sparse, fuzzy, or patchy fur coverage that may resemble hairlessness by adulthood. At the molecular level, the Rex phenotype arises from a 7-base pair deletion at the splicing acceptor site of intron 1 in the keratin 71 gene (Krt71), which disrupts normal mRNA processing and leads to an altered essential for hair shaft formation. This change primarily affects the alpha-helical rod domain of the KRT71 protein, impairing filament assembly in hair follicles without causing broader physiological deficits in heterozygotes. The mutation's semi-dominant means that breeding two heterozygous Rex rats yields approximately 25% homozygous with intensified curl but reduced hair density, 50% heterozygous with standard Rex waviness, and 25% wild-type smooth-coated rats. Breeders typically select against homozygous production to maintain desirable coat aesthetics, as double Rex rats can develop thin pelage around 6-8 weeks of age. Rex rats are widely utilized in the fancy rat pet trade for their appealing curly appearance, available in various colors and patterns, and have been incorporated into standardized strains for exhibition and companionship. In laboratory settings, they serve as models for studying keratin-related dermatological processes, including hair growth cycles and follicle morphogenesis, due to the well-characterized Krt71 alteration. No major health issues, such as immune deficiencies or reduced lifespan, are associated with the heterozygous Rex trait, though homozygous individuals may require careful monitoring for skin sensitivity.

In Birds

Feather effects

In birds, rex-like mutations produce curly feather phenotypes characterized by frizzling or waviness, resulting from structural alterations in the feather's barbules and rachis that parallel the helical curling of mammalian hair shafts. These changes disrupt the normal flat-lying arrangement of feathers, causing them to curl outward and upward away from the body, which creates a distinctive, ruffled appearance. Unlike straight feathers that interlock efficiently, the modified barbules in affected feathers fail to hook properly, leading to a looser overall . The genetic basis for these curly feather traits involves mutations in keratin-associated genes, particularly the α-keratin KRT75, which encodes a structural protein essential for integrity. In chickens, a dominant in KRT75—specifically a 13-base pair insertion at the acceptor splice site of intron 7—results in during transcription, producing a truncated protein that alters filament assembly and leads to rachis . This causes overexpression of the faulty in follicles, weakening the central shaft (rachis) and inducing barb curvature. Similar keratin disruptions, such as a novel deletion in the related KRT75L4 , have been identified in certain Chinese populations, further confirming keratin's role in feather frizzling across avian lines. In other domesticated birds like , a distinct recessive curly affects texture independently of KRT75, though it similarly alters barbule alignment for a wavy . These rex-analogous traits generally reduce preening efficiency, as the curled feathers trap more dirt, debris, and moisture, complicating birds' ability to maintain cleanliness through natural grooming behaviors. Despite this, the phenotypes hold significant ornamental value in domesticated birds, where emphasizes their aesthetic appeal for exhibition purposes. Unlike mammalian rex mutations that primarily impact density and texture for insulation, avian feather alterations have minimal effects on , though they compromise thermal regulation by preventing proper feather overlap and air trapping—resulting in poorer cold tolerance but enhanced heat dissipation in warm environments. No standardized "rex" exists for birds; instead, terms like "frizzle" or "curly" denote these traits in such as chickens, , and pigeons.

Known examples

One prominent example of a rex-like in birds is the frizzle trait in , characterized by curled due to a in the α-keratin gene KRT75, commonly denoted as the F gene. This causes the rachis and barbs to curl outward, giving the a distinctive frizzled appearance. The frizzle chicken originated in and was documented in the as early as the , with for exhibition purposes intensifying in the and during the , where it became popular in shows by the 1870s. Another example is the crest mutation in pigeons, where a nonsynonymous in the EphB2 leads to upward-growing s on the head and neck, producing a curly or ruffled crest . This dominant was identified in a 2013 study at the , which sequenced the rock pigeon and linked the EphB2 variant to altered orientation in crested breeds derived from the rock pigeon (Columba livia). Such traits have been selectively bred in ornamental pigeons since the , though they remain rare in wild populations. In Asiatic breeds like the , a recessive in the PDSS2 (also known as hookless or h) results in silky, downy s lacking proper barbules, producing a fluffy, fur-like that is distinct from the structural curling seen in frizzles. This trait contributes to the breed's fluffy , though it is distinct from the structural curling seen in frizzles. Overall, rex-like feather s in birds have been subject to for ornamental purposes since the 1800s, primarily in domestic lines, with such variants being exceedingly rare in wild avian populations due to their lack of adaptive value. The frizzle exhibits incomplete dominance, where heterozygotes (Ff) show moderate curling, while homozygotes (FF, known as frazzles) display extreme frizzling but suffer health complications, including enlarged hearts and elevated heart rates linked to higher metabolic demands. These issues, first documented in early physiological studies, often limit breeding viability in homozygous individuals.

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