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Inheritance of melanocytic lesions and their association with the white colour phenotype in miniature swine
Author(s) -
Volker Müller,
; Wanke,
Distl
Publication year - 2001
Publication title -
journal of animal breeding and genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.689
H-Index - 51
eISSN - 1439-0388
pISSN - 0931-2668
DOI - 10.1046/j.1439-0388.2001.00280.x
Subject(s) - biology , allele , penetrance , melanoma , phenotype , locus (genetics) , genetics , gene , pathology , medicine
A line of Munich Miniature Swine (MMS) Troll showing a high incidence of spontaneous benign and malignant cutaneous melanocytic lesions has been developed since 1986. The inheritance of cutaneous melanocytic lesions was studied by establishing the F 1 ‐, F 2 ‐ and reciprocal B 1 ‐generations with one melanoma MMS‐Troll boar and four unaffected German Landrace sows as founders. A total of 176 animals were available, 27 in the F 1 ‐, 111 in the F 2 ‐, 19 in the B 1‐DL ‐, and 14 in the B 1‐Troll ‐generation. Benign melanocytic lesions were observed in 42% of F 1 ‐, 18% of F 2 ‐, 11% of B 1‐DL ‐ and 50% of B 1‐Troll ‐animals. Malignant melanomas developed in 3.6% of F 2 ‐ and 7.1% of B 1‐Troll ‐animals, although no animal with white coat colour was affected. A mixed major gene model with arbitrary gene action explained the segregation of benign lesions sufficiently well. For melanomas a mixed major gene model required additional dominant acting suppressor loci to obtain a sufficient fit to the data. An influence of SLA haplotypes on the penetrance of melanocytic lesions was not evident. The association analysis of the white phenotypes strongly indicated that the dominant allele I at the I‐locus suppresses malignant melanocytic lesions. 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.