Isolation of the ovine agouti coding sequence.
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Biomedical subjects
Publications and source records attributed to M R Fleet.
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Black-grey pigmented skin spots, some of which contained pigmented wool fibres, were observed in a flock of 8.5-year-old white Merino ewes. The spots were concentrated along the backline and increased in number following shearing, suggesting exposure to sunlight to be of importance in the development of these non-congenital pigmented skin spots in genetically white Merino sheep. To test the effect of ultraviolet light, white Merino sheep, ranging in age from 3 to 8 years, had a closely clipped midside area of wool-bearing skin irradiated on each of 28 consecutive days. Pigmented skin spots developed in 6 of the 16 white Merino sheep irradiated. Spots first appeared after 10 days of irradiation, the number subsequently increasing with time, and two skin spots were found to contain sparse numbers of black-grey pigmented wool fibres. Histological examination showed both the naturally occurring and irradiation-induced pigmented skin spots resulted from an increase in both number and activity of melanocytes localized along the epidermal-dermal border of the epidermis. With time, the melanocytes were observed to have entered, to varying depths, the outer-root sheath of follicles still producing white wool fibres. These ultraviolet-light-induced changes to epidermal melanocytes in white Merino sheep presumably occur due to alterations within the local tissue environment in which the melanocytes lie.
The distribution and character of melanocytes in the wool-bearing skin of Merino sheep of known genotypes were examined by light and electron microscopy. In black Merino sheep (ww, homozygous recessive), melanocytes were localized within three regions of the skin: epidermal-dermal border, outer root sheath and follicle bulb. Melanocytes within these regions were found to be actively producing melanin, had numerous dendritic extensions and were able to transfer melanin to adjacent keratinocytes. In a black Merino sheep whose fibres were white due to an experimentally induced copper deficiency the melanocytes were amelanotic. In contrast, for both WW (homozygous dominant) and Ww (heterozygous) white Merino sheep melanocytes were observed only at the epidermal-dermal border of the epidermis. The melanocytes appeared also to differ in character containing less melanin, appearing less dendritic in shape and having a reduced ability to transfer melanin to adjacent keratinocytes. The gene for white fleece (W), therefore, appears able to regulate pigmentation in Merino sheep, at least in part, by controlling the location and activity of melanocytes within the wool-bearing skin.
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This report introduces the second form of true albinism to be documented in sheep, which appears mild enough not to cause serious undesirable side effects yet apparently effective enough to have the potential for general usage in the sheep industry. Based on the matings conducted to date, the albinism is inherited like an autosomal recessive. Histochemical tests reveal a defective melanin synthesis involving a block to the conversion of tyrosine to dopa but not the subsequent reactions that lead to melanin. The enzyme tyrosinase is a product of the C locus and catalyzes the conversion of tyrosine to dopa and the following reaction (dopa to dopaquinone). Therefore, it is proposed that the albinism arises from a gene in the C locus that encodes a defective tyrosinase. The gene is provisionally named albino marrabel, the gene symbol is cmar, and the locus allele symbol is Ccmar.