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New mutation causing jaundice in mice.

A M Saxton, E J Eisen, B H Johnson

    The Journal of Heredity
    |November 1, 1985
    PubMed
    Summary
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    A novel mouse mutant exhibits jaundice due to elevated unconjugated bilirubin shortly after birth. This genetic condition, hyper-unconjugated bilirubinemia (hub), also affects adult male fertility and maternal performance.

    Area of Science:

    • Genetics
    • Animal Models
    • Biochemistry

    Background:

    • Jaundice in newborns can result from various genetic and physiological factors.
    • Understanding the genetic basis of bilirubin metabolism is crucial for diagnosing and treating related disorders.
    • Existing mouse models for hemolytic anemia do not fully explain all forms of neonatal jaundice.

    Purpose of the Study:

    • To characterize a newly identified mouse mutant exhibiting neonatal jaundice.
    • To determine the genetic basis and allelic relationships of this mutant.
    • To investigate the physiological consequences of the mutation in adult mice.

    Main Methods:

    • Phenotypic analysis of mutant mice from birth to adulthood.
    • Allelism tests with known hemolytic anemia and jaundice mutants.

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  • Serum bilirubin level measurements.
  • Reproductive performance assessment in adult male and female mutants.
  • Genetic mapping to identify the responsible gene.

    • Main Results:

    • A new autosomal recessive mutant causes jaundice in mice within 24 hours postpartum due to increased unconjugated bilirubin.
    • The mutation is not allelic with previously identified hemolytic anemia mutants (sphha, ja, nb, sph, sph2Be).
    • Adult male mutants display reduced testes size and infertility, while females show reduced maternal performance.
    • The gene responsible for this condition is proposed to be named hyper-unconjugated bilirubinemia (hub).

    Conclusions:

    • The novel 'hub' mutation in mice provides a new model for studying unconjugated hyperbilirubinemia.
    • This model can aid in understanding the genetic regulation of bilirubin metabolism and its impact on reproduction.
    • Further research into the 'hub' gene may reveal insights into human disorders of bilirubin processing.