Articles | Volume 43, issue 3
https://doi.org/10.5194/aab-43-277-2000
https://doi.org/10.5194/aab-43-277-2000
10 Oct 2000
 | 10 Oct 2000

Segregation von Pigmentzellanomalien bei Kreuzungen zwischen dem Münchener Miniaturschwein Troll und der Deutschen Landrasse

S. Müller, R. Wanke, W. Hermanns, and O. Distl

Abstract. Title of the paper: Segregation of melanocytic lesions in crosses among the Munich Miniature Swine Troll and German Landrace
Since 1986, a line of Munich Miniature Swine (MMS) Troll showing a high incidence of spontaneous benign and malignant cutaneous melanocytic lesions has been established at the University of Munich. In order to study me inheritance of cutaneous melanocytic lesions in the Munich Miniature Swine Troll, we established the F1-, F2-, BIDL-, and BITroll-generations, starting with one melanoma-bearing MMS Troll boar and four non-affected sows of the German Landrace (DL) as founder animals. A total of 176 animals were available, 27 in the F1-, 111 in the F2-, 19 in the B|DL-, and 14 in the BITroll-generation. Benign melanocytic lesions with two distinct forms of basal melanocytic hyperplasia or nests of hyperplastic melanocytes like in human junctional nevus were observed in 10 (41,7%) F1-, 20 (18%) F2-, 2 (10,5%) BIDL-, and 7 (50%) BITroll-animals. Malignant melanomas were found in four (3,6%) F2- and one (7,1%) BITroll-animals, but did not occur in the F1- and BIDL-generations. The observed segregation pattern suggests a different mode of inheritance for benign melanocytic lesions and melanomas, respectively. An influence of SLA haplotypes could not be observed. However, a significant influence of coat colour on the occurence of melanoma could be found in the F2-generation. While around 65% of F2-animals had the German Landrace dominant white colour, melanomas were only found in black and red animals. Benign lesions of the junctional nevus type, too, were only found in black animals. A possible explanation is the lack of melanocytes in the skin of dominant white pigs caused by a mutation of the KIT-gene, which leads to a failure of melanoblast migration and development

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