The Journal of Heredity 1984:75(1):2-7
© 1984 The American Genetic Association 75:2-7
research-article |
A tiger mouse and relatives
Variants caused by an activated transosable element?
Department of Genetics, University of Cambridge Downing Street Cambridge CB2 3EH, England
Department of Zoology, University College London, England
Abstract
In a laboratory-bred population of wild Peruvian house mice, one male had an excessive rate of non-pairing of the X and Y chromosomes. After crossing him with laboratory stock mice, a mouse of very unusual phenotype appeared from a yellow (AyA) mother. He was yellow with black dorsal stripes; hence Tiger. He was mated to many females, and inbred F2 and F3 generations were raised. There were no more tiger phenotypes, but his F1 contained an excess of black-and-tans over yellows, showing him to be a gonosomic mosaic Ayat/atat; the homozygous cell line probably arose from the heterozygous one. The mitotic karyotype was normal. Some of Tiger's mates were of known allozyme types and their progeny were scored. The allozyme segregation were normal, except at the Es-3 locus (esterase-3), for which Tiger was typed as homozygous. Several unusual events among Tiger's close relatives included a mutation to an unstable pattern mutant, three probable translocations, and several cases of somatic defect. All unusual mice derived from Tiger's yellow mother, whose genome was one-quarter Peruvian. Yellow is associated with an ecotropic murine leukemia virus. The Peru genome is characterized by a high occurrence of mutation and aberrant karyotypes. It is suggested that something from the Peru genome in Tiger's mother caused instability of the DNA sequence associated with yellow, with related disturbance at different locations thereafter. The nature of this instability, and of the Peru genome, is discussed.