The inheritance of spontaneous amyloidosis development in mice: A model for hereditary threshold metabolic disorders

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Abstract
To study the inheritance of spontaneous amyloidosis development in mice, we crossed the LLC strain (with a high incidence) with the A/J strain (with a low incidence) and with the HLC strain (with a zero incidence of amyloidosis). We produced the F1 and a backcross generation to each parental strain in each cross. Examination of the spleen, liver, and kidneys of each mouse for the presence of amyloid was made between age 15 and 18 months. The data fit neither a dominant nor a recessive single gene hypothesis for the development of amyloidosis. In consideration of amyloidosis as a hereditary threshold character, we developed an additive gene model. Subsequently, a test for fitness of the observed percentages to the expected percentages in the backcross generations was made according to this model. The observed percentages of amyloidosis in the spleens, livers, and individual mice agreed with the expected percentages in the LLC × A/J crosses but not in the LLC × HLC crosses. Therefore, we conclude that for the development of amyloidosis, a difference exists at one locus between LLC and A/J and at more than one locus between LLC and HLC. The probability of development of amyloidosis in an individual depends on the effects of the genes at these loci. For hereditary metabolic disorders that cannot be explained by either a single dominant or recessive gene hypothesis, this genetic model may be useful to test whether the development of the disease is due to additive effects of genes.

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