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Genetic basis of susceptibility to splenic lipofuscinosis in mice

Published online by Cambridge University Press:  14 April 2009

D. N. Crichton
MRC Clinical and Population Cytogenetics Unit, Western General Hospital, Edinburgh EH4 2XU, Scotland
J. G. M. Shire
Institute of Genetics, University of Glasgow, Glasgow G11 5JS, Scotland Department of Biology, University of Essex, Colchester CO4 3SQ, England
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Spleens with black pigment in them were found in 4–57% of mice from 17 stocks, all sublines of C57BL or with significant C57BL ancestry. Splenic lipofuscinosis was absent from 16 stocks, including three C57BL/6By × BALB/cBy recombinant - inbred lines. Progeny testing showed all C57BL/6J mice to be equally likely to develop black spleens. The penetrance of lipofuscinosis differed between sublines but not between the sexes or between laboratories. Susceptibility to lipofuscinosis showed dominant, autosomal, inheritance in F1 hybrids. Observations on backcrosses and on recombinant inbred lines and their intercrosses indicated the existence of two genetic factors. Splenic lipofuscinosis was prevented either by a deficiency of melanin or by homozygosity for a non-C57BL allele close to the c-p region of chromosome 7. The presence of a C57BL allele at a locus on another chromosome is necessary for lipofuscinosis to occur.

Research Article
Copyright © Cambridge University Press 1982



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