The overall appearance of mice homozygous for either the Scd1ab-2J or the Scd1ab-J (no longer available) allele includes slightly hunched posture, dry, scaly skin, thin fur sometimes detectable by 7 days of age, and small eyes with encrusted eyelids stuck shut. They have hypoplasia of the sebaceous glands and other hair follicle abnormalities that result in scarring alopecia. These mice have a paucity of adipose tissue, thin subcutis, and a distinctive odor. Hepatic cholesterol ester and triglyceride synthesis was shown to be deficient in Scd1ab-J homozygotes and could not be restored through diet. Early studies of skin lipids in the original asebia mutant ((Scd1ab) revealed a deficiency in wax esters, wax diesters, and sterols esterified with very long-chain fatty acids along with an increase in free sterols. (Wilkinson and Darasek, 1966; Sundberg et al., 1994; Zheng et al. 1999; Miyazaki et al., 2000; Sundberg et al., 2000) Mice homozygous for the Scd1ab-2J allele showed greater dermal inflammatory infiltrate in the skin and thicker epidermis than did Scd1ab-J mice. Scd1ab-2J homozygotes show an increased transepidermal water loss and corresponding ad libitum intake of water that was not seen in Scd1ab-J homozygotes. For a thorough description see Sundberg et al., 2000 and Sundberg, 1994.

Mice homozygous for the Scd1ab-2J allele show slightly hunched posture, dry, scaly skin, thin fur, and small eyes with encrusted eyelids stuck shut. They have hypoplasia of the sebaceous glands and other hair follicle abnormalities that result in scarring alopecia. They also have a paucity of adipose tissue, thin subcutis, and a distinctive odor.

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