I get asked at least once a week if I breed hairless or ‘patchwork’ rats, and each and every time my answer is a big fat no, I don’t purposely ever set out to breed disabled rats, and HAIRLESS RATS ARE DISABLED, no matter how you dress it (or them) up.
A summary of the common reasons why, and the issues different hairless genes can have. Not nice at all and never something I would set out to breed.
Rowett Nude/rnu/Athymic Hairless:
Discovered at the Rowett Research Institute in Aberdeen, UK in 1953.
Appearance: Whiskers are present but bent. Short hairs are found on the head, and to a lesser extent on the rest of the body. From age 2 to 6 weeks the skin may seem covered with brownish scaly flakes, rats later become smooth and hairless. Later, rats may grow a covering of hair and lose it again (Festing et al. 1978)
Other effects: nude rats have no functioning thymus. Instead they have brown fat tissue and a small and highly abnormal thymus rudiment. The lack of the thymus leads to immunodeficiency (no cell mediated immune response e.g. T-cells). Nude rats grow at only 60-80% of the rate of normal rats (Festing et al. 1978)
Patchwork rats may owe their appearance to an allelic variation of Rowett nude as well. The name and symbol has changed over the years, so it may be listed in journals as Whn which stands for “Winged-helix nude”, or Foxn1.
(Festing MFW, D May, TA Connors, D Lovell, S Sparrow. 1978. An athymic nude mutation in the rat. Nature. 274. 365- 366.)
Appearance: Shorn, a recessive mutation causing hairlessness, was discovered in 1993. Shorn rats display a very sparse, patchy coat throughout their lifetimes. By six weeks, they have a sparse short coat on the body but not on the face, by eight weeks the body is again nearly hairless and short, sparse hair appears on the face in a mask pattern. Adults may retain a sparse mask of short, sparse mask of hair on their face and patchy, ragged hair on their rumps and bellies. They have short, kinky whiskers (Moemeka et al. 1998).
Other effects: Shorn rats develop abnormal hearts and kidneys which are yellow and bumpy instead of red and smooth. They tend to be smaller than normal rats and they die prematurely, at around 12-14 months of age (Moemeka et al. 1998).
Fuzzy: (Estimated to be the most popular type in the UK)
Appearance: Homozygous infant rats have curly or twisted whiskers at birth. Their first coat is short, rough, and the hairs are broken, which gives the coat a wavy appearance. This short coat may last through one or two hair cycles, but by 2 months of age most mutant rats have only sparse hair and a fuzzy appearance, or no hair at all. By six months, all homozygous rats are usually smooth-skinned and remain so thereafter (Palm and Ferguson 1976, Ferguson et al. 1979, Marit et al. 1995)
Kidney failure: Fuzzy rats suffered from chronic, progressive nephrosis, or nephropathy, which shortened their lifespan to 16.6 months in males and 20.4 months in females.
Details: Chronic, progressive nephrosis means the thickening of the basement membrane of the kidney with protein cases, and it leads to kidney failure. Chronic nephrosis progresses differently in male and female fuzzy rats. Generally, males are more affected, at an earlier age, than females are, though by old age all fuzzy rats had the condition. Specifically, chronic nephrosis started around 8 weeks of age in both sexes, but neither sex was obviously affected for several months. However, at 21 weeks of age almost all the males had mild nephropathy, which became diffuse nephropathy in of all the males by 32 weeks of age. Females remained healthier for longer, as they did not show diffuse nephropathy until 52 weeks of age, and even then it was in only half the females. By old age, however, all rats had progressive nephrosis.
In the laboratory, the fuzzy rat has some health issues that must be taken into consideration. The females tend to have irregular cycles, coming into heat approximately every 8 to 14 days (at least double that of a normal rat’s 4 days). In some lines, the females have trouble lactating. In both sexes, the adrenals and kidneys are enlarged, and they often succumb to kidney disease by 18 months of age. Heterozygous rats, that is, rats which have normal fur and carry one copy of the fuzzy mutation, can have slightly enlarged kidneys and adrenals as well.
Longevity: In one longitudinal study of the health of fuzzy rats all males and 80% of the females were debilitated by kidney failure and were eventually euthanized. Males averaged 16.6 months (range: 12-20 months), and females averaged 20.4 months (range: 17-26 months) at time of death. This age at death is younger than normal rats, indicating that fuzzy rats have a decreased lifespan (Marit et al. 1995).
Tumors: The tumor incidence in fuzzy rats was similar to that in normal rats (70% females and 25% males developed tumors, almost all of which were benign), but fuzzy rats developed their tumors at an earlier age than normal rats (Marit et al. 1995).
Adrenal glands: cystic degeneration of the adrenal gland (replacement of cortical cells by cyst-like spaces containing blood or serum). Females are more affected than males. This condition was rare and mild in young fuzzy rats, but by old age 100% of females had moderate to severe lesions, and 35% of males mild and a few moderate lesions (Marit et al. 1995).
Skin: The skin of fuzzy rats has fewer, smaller, poorly developed follicles. Frequently the lumen of the follicle is enlarged and completely filled with keratin. These accumulations of keratin form cysts in the skin. The skin of fuzzy rats has a slightly thicker stratum corneum (Palm and Ferguson 1976, Ferguson et al. 1979, Marit et al. 1995).
Hair: Hair shafts of fuzzy rats are smaller and do not contain the medulla. The corniform layer is slightly thicker and more loosely arranged than normal. Sebaceous glands are more prominent (Palm and Ferguson 1976, Ferguson et al. 1979, Marit et al. 1995).
Other: Mild myocardial degeneration (cardiomyopathy), retinal atrophy (Marit et al. 1995).
Genetics: The exact gene that is affected by the fuzzy mutation is not known. However, the fuzzy mutation has been mapped to a location on Chromosome 1 in the rat, and there are many good potential gene candidates at that spot. One of the most compelling genes that may be involved is the fibroblast growth factor receptor 2 gene (Fgfr2) which is expressed in hair follicles (Ahearn et al. 2002).
Charles River Hairless:
Appearance: Charles River "hairless" rats have abnormal keratinization of the hair shaft, and the formation of a thick, dense layer of dead skin cells (corneocytes) in the skin. This thick layer prevents the poorly keratinized hair shaft from penetrating to the skin surface. The hair follicles degenerate over just a few days, and by day 12 the skin has mostly degenerated hair follicles with abnormal or broken hairs.
Other effects: Charles river hairless embryos are not as viable as normal rats, resulting in reabsorption. Mutant mothers produce normal sized litters (about 9 pups) but only raise a few to weaning age (about 2 pups). Interestingly, hybrid mothers carrying one Charles River allele and one fuzzy allele (CRhr/fz, see photo) had much more success rearing their litters (successfully raised 25 out of 27 offspring) (Ahearn et al. 2002).
Genetics: The Charles river hairless mutation annuls cell proliferation in the hair matrix and affects keratinocyte differentiation in the hair follicle and in the skin (Panteleyev and Christiano 2001, Ahearn et al. 2002).
(Ahearn, et al. The Charles River “Hairless” Rat Mutation Maps to Chromosome 1: Allelic With Fuzzy and a Likely Orthologue of Mouse Frizzy. The Journal of Heredity 2002:93(3): 210-213.)
This mutation, symbol vb, is a recessive hairless mutation which also causes a lack of whiskers. Females are unable to lactate. This form can be identified at birth due to the complete lack of whiskers and reduced facial hair. The nails also tend to easily break off even in newborns and spontaneously shed through the lifetime of the rat.
Skin: These rats are prone to skin crusting due to blisters between the layers of skin, and females cannot nurse young at all due to the blistering of the nipples and surrounding skin.
Overall body size is smaller and lifespan is reduced.
In 1985 a male hairless rat mutant was discovered in a breeding colony of Sprague Dawley rats at the Hirosaki University in Japan. Bred against known hairless mutations it was found to be non-allelic; later it was identified as a mutation on chromosome #7 and given the symbol of krt83; the symbol stands for keratin because in this rat, the genes that code for keratin in the hair were not expressed. In addition to hair loss, the females have underdeveloped mammary glands and are unable to nurse their young.
(Nanashima, Naoki, Et Al. The Hairless Phenotype of the Hirosaki Hairless Rat Is Due to the Deletion of an 80-kb Genomic DNA Containing Five Basic Keratin Genes. J. Biol. Chem., Jun 2008; 283: 16868 - 16875)
The rats affected by this mutation (lah/lah), have generalised hairlessness, with some partial hair growth, particularly on the head; the hair is also quite rough and has a distinct shape when viewed close up which is where the name comes from ( it is ‘lance like’, thick at the distal end and thin at the bottom). These rats also have thicker, stiffer skin. It’s been mapped to chromosome 18.
A dominant form of hairlessness has been identified in the rat and given the symbol Ht. Heterozygotes have hypotrichosis and whiskers are lightly wavy. The Homozygotes have atrichosis; their whiskers are very curled and short whiskers. The homozygotes die before weaning. This mutation is mapped to chromosome 10, but it is not allelic to Rowett, nor does it have an abnormal thymus like the Rowett does. (Akimoto T, Suzuki H, Nakama K, Suzuki K. Dominant Hairless Gene (Ht) is Located on Rat Chromosome 10. Experimental Animal, Volume 42, No.2, April 1999)
Discovered in 1973 in the USA, 'bald' rats begin to lose their hair at approximately three weeks of age and by five weeks of age, the skin was devoid of all general body hair except for the whiskers, and the skin became extremely wrinkled at two months of age.
The bald condition was a simple recessive character (ba); homozygous animals lost hair (visible hairless) and heterozygous (carrier) ones did not.
Skin issues: Aged bald animals showed spontaneous tumors of the thymus, pituitary, testis, uterus, mammary gland, and skin. The incidence of skin tumors was much higher than those of tumors of other origins. Histologically, follicular cysts were observed in a large number of those tested, from three months of age onward. (Characteristics of a new hairless mutation (bald) in rats. Inazu M, Kasai K, Sakaguchi T)
Breeding and Fertility: The bald females reached sexual maturity around eight weeks of age and birthed normally, but failed to nurse their young. The incapability of supplying sufficient milk supposedly resulted from the mammary glands that involuted after delivery, and newborns often died due to this.
Other effects: The bald animals consumed more food but showed lower values for body weights, plasma triglyceride, and epididymal adipose tissue amount than the haired animals, and did not reach the same adult weights as their furred counterparts. In addition, the bald males had brown adipose tissue in the interscapulum which was histologically activated as in newborn animals.
Appearance: Like the other hairless mutations, naked also affects the whiskers, which are twisted and hair growth is little to non-existent as youngsters. These rats are smaller than their normally furred siblings and the Naked rat’s juvenile coat is quickly lost at three weeks of age. The newly exposed skin is generally flaky, yellow and dry, but it later becomes pink and soft. Some light fuzz comes in after four weeks, only to be quickly lost again. This cycle repeats for several months.
Naked is epistatic to (“masks”) the “hairless” mutation (as described by Castle and King) from the age of six weeks onward, by preventing the adults from developing the thickly wrinkled skin associate with it.
Fertility and lactation problems are frequently reported.
(Kim H, Panteleyev AA, Jahoda CA, Ishii Y, Christiano AM. Genomic organization and analysis of the hairless gene in four hypotrichotic rat strains. Mamm Genome. 2004 Dec;15(12):975-81)
Rats have ragged and semi-hairless juvenile coats. Most of the hair on the back is transitionally lost around 5 weeks of age and re-covered with ragged hair thereafter. Eyelids become thickened at 3 weeks of age. Sebaceous glands are enlarged & increased in number on the back, and sebaceous cysts are very common.
(Noguchi J, Ajisawa C, Ikadai H, Imamichi T. 1990. Ragged—a new rexoid mutant rat with large sebaceous gland. Jikken Dobutsu. 39(3):383-8.)
Sparse and Wavy (swh/swh)
Homozygotes have sparse and wavy hair, due to hair follicles being Wavy reduced in both number and size. Has associated hypoplasia of the sebaceous glands and the subcutaneous fat tissue. Weight gain is impaired as is overall growth and lifespan.
Female rats have hypoplastic mammary glands and cannot lactate. Spontaneously arose in the WTC inbred rat strain colony at the National Cancer Center Research Institute in 1998.
(Kuramoto, et al. Sparse and Wavy Hair: A New Model for Hypoplasia of Hair Follicle and Mammary Glands on Rat Chromosome 17. Journal of Heredity 96: 339-345. )
I realise that people love their appearance, being a bit ‘different’, but the breeding of these poor buggers honestly isn’t worth it, so many rats suffer in the long run, and I honestly cannot support the breeding of them.
I urge others to also consider their own thoughts on them and possibly re-asses based on ethical considerations and the further implications that can be involved.