# Skinbase

##### Mouse Skin and Hair Database

## Asebia (Stearoyl-Coenzyme A Desaturase 1)

- Telogen stage hair follicles from a one month old female DBA/1LacJab-Scd1<ab2J>/Scd1<ab2J> mouse. The follicles extend deep into the hypodermal fat layer close to the panniculus muscle and are equal in length to the Anagen.
- The normal sebaceous gland is part of the hair follicle; large pale clusters of cells with fine clear vacuoles of consistent size produce lipid and enzymes critical to the maintenance of normal skin and hair follicles. This tissue is from an adult DBA/1LacJ +/+ (control) mouse.
- Sebaceous glands are present and so these mice are hyposebic rather than asebic. The epidermis is thicker and anagen follicles longer than normal. This tissue is from an adult DBA/1LacJ-Scd1<ab2J/Scd1<ab2J> mouse.
- Hypoplastic sebaceous gland in an adult DBA /1LacJ-Scd1<ab2J>/Scd1<ab2J> mouse.
- Hair follicles rupture and cause a foreign body granuloma in an adult DBA/1LacJ-Scd1<ab2J>/Scd1<ab2J> mouse.
- Skin from a 14 month old male ABJ/Le Scd1<abJ>/Scd1<abJ> asebia mutant mouse. The long anagen hair follicle appears to be normal. Note the small sebaceous gland. 100X magnification.
- This is a normal anagen hair follicle taken at 100X from an ABJ/Le +/+ (control) mouse for the asebia J mutation. Note the normal sebaceous gland.
- 400 X magnification of a normal sebaceous gland from an ABJ/Le +/+ (control) mouse.
- Hypoplastic sebaceous gland from an ABJ/Le Scd1<abJ>/Scd1<abJ> asebia mutant mouse. Note the dilated infundibulum.
- ABJ/Le Scd1<abJ>/Scd1<abJ> asebia mutant mouse 250X magnification. Note the fibrous tracts perpendicular to and extending from the epidermis. These are follicular scars (cicatrical alopecia).
- ABJ/Le Scd1<abJ>/Scd1<abJ> asebia mutant mouse skin 400X magnification. Note the fibrous tracts perpendicular to and extending from the epidermis. These are follicular scars (cicatrical alopecia).

The asebia hairless mutation arose as a spontaneous mutation in the stearoyl-Coenzyme A desaturase 1 gene in the BALB/cCrglGa strain. Homozygotes may be recognized at 7 days of age by retarded growth of the coat. Alopecia increases, and at adulthood the hair is very sparse. Homozygotes are viable and fertile, but fertility of females is somewhat reduced. Hyperplasia of the cellular layers of the skin is apparent at birth and increases markedly with age. Fibroblasts in the dermis are morphologically abnormal, and collagen and elastin show alterations. Hair follicles are initially normal, but soon become abnormal, with cells of the inner root sheath plugging the hair canal and adhering to the emerging hair. Sebaceous glands are present but differentiate abnormally, with abnormal smooth endoplasmic reticulum and mitochondria, and few lipid droplets. Meibomian glands are also defective. Results of reciprocal transplantation of skin between normal and mutant mice suggest that some diffusible substance synthesized by normal skin can stimulate hair growth and alleviate the hyperkeratosis characteristic of the mutant skin. The skin is deficient in esterified sterols and waxes, but rich in free sterols. Homozygotes for targeted and spontaneous mutations exhibit alopecia, scaly skin, sebaceous gland hypoplasia, impaired ocular lubrication and synthesis and storage of triglycerides, higher lipid oxidation, reduced growth, and lower fertility in females.
A spontaneous, autosomal, recessive mouse mutation exhibiting mild scaly skin, progressive scarring alopecia, slightly runted growth, and photophobia arose at The Jackson Laboratory in 1993 in the inbred mouse strain DBA/1LacJ. Because this mutant mouse showed genetic, anatomical, and laboratory similarities to the asebia mutation, crosses were done between the new mutant and mice carrying the asebia-J allele. Because the F1 offspring were affected, indicating the two mutants were allelic, the new mutation was named asebia-2J. Careful histological analysis of skin development of mice homozygous and heterozygous for either asebia-J or asebia-2J revealed that both types of mutant mice are very similar regardless of their background. Notable histopathological features of mice homozygous for either allele included extreme sebaceous gland hypoplasia, abnormally long anagen follicles, retained inner root sheath, hair fiber perforation of the bulb region as anagen progressed to catagen, foreign body reaction to hair fibers in the dermis, and progressive follicular replacement by scarring. A new pathogenetic hypothesis based on the importance of the sebaceous gland in hair fiber sheath dissociation was suggested by Sundberg et al. (2000): in the absence of a functional sebaceous gland the hair follicle is destroyed. The cutaneous lesion of this mutant mouse underscores the importance of the sebaceous gland to follicular biology and presents an animal model for studying the human scarring alopecias(now called cicatrical alopecias), which characteristically begin with sebaceous gland ablation.

### References

Gates AH; Karasek M, Hereditary absence of sebaceous glands in the mouse., Science 1965;148():1471-1473
Josefowicz WJ; Hardy MH, The expression of the gene asebia in the laboratory mouse. I. Epidermis and dermis., Genet Res 1978 Feb;31(1):53-65
Josefowicz WJ; Hardy MH, The expression of the gene asebia in the laboratory mouse. 2. Hair follicles, Genet Res 1978;31():145-55
Josefowicz WJ; Hardy MH, The expression of the gene asebia in the laboratory mouse. 3. Sebaceous glands., Genet Res 1978;31():157-166
Sundberg JP, Boggess D, Sundberg BA, Eilertsen K, Parimoo S, Filippi M, Stenn K. Asebia-2J (Scd1<ab2J>): a new allele and a model for scarring alopecia. Am J Pathol. 2000 Jun;156(6):2067-75.
Hu CC; Qign K; Chen Y, Diet-induced changes in stearoyl-Co A desaturase 1 expression in obesity-prone and -resistant mice., Obes Res 2004 Aug; 12(8):1264-70.
Matsusue K; Gavrilova O; Lambert G; Brewer HB Jr; Ward JM; Inoue Y; LeRoith D; Gonzalez FJ, Hepatic CCAAT/enhancer binding protein alpha mediates induction of lipogenesis and regulation of glucose homeostasis in leptin-deficient mice., Mol Endocrinol 2004 Nov; 18(11):2751-64

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