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The Journal of Heredity 1985:76(6):441-446
© 1985 The American Genetic Association 76:441-446

research-article

New mutation causing jaundice in mice

A. M. Saxton, E. J. Eisen, B. H. Johnson, and J. G. Burkhart

The authors are, respectively, assistant professor in the Department of Experimental Statistics, Louisiana State University, Baton Rouge, LA 70803; professors in the Department of Animal Science, North Carolina State University, Raleigh, NC 27695; and research chemist, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. The authors thank Dr. S. E. Bernstein, the Jackson Laboratory, Bar Harbor, Maine, for supplying the heterozygous males used in the allelism tests, and Zola Turner for technical assistance. Paper no. 9738 of the journal series of the North Carolina State University Agricultural Research Service, Raleigh, NC 27695.

Abstract

A new mutant causing jaundice in mice is reported. Allelism tests indicate that it is not allelic with known hemolytic anemia mutants in mice [hemolytic anemia (sphha), jaundiced (ja), normoblastic anemia (nb), and spherocytosis (sph and sph28e)]. The jaundiced condition appears in young mice at about 24 hours postpartum and is due to a major increase in unconjugated bilirubin in serum compared to normal controls. Adult mutant mice are not jaundiced and bilirubin levels do not differ from normal mice. Adult male mutants have reduced testes size and no viable sperm. Female mutants are fertile but overall maternal performance is reduced as indicated by increased mortality and reduced growth rate of pups. Genetic tests indicate that a single autosomal recessive gene is responsible for the condition. We propose that the mutant be designated hyper-unconjugated bilirubinemia, with the gene symbol hub.


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