In this report, we assign fsn to distal chromosome 17 and characterize the anemia. There is compensatory enlargement of the heart, liver, and spleen by 8 weeks of age, whereas the thymus is less than one half normal weight. Erythrocyte membrane fragility is normal.
Hemolysis is indicated by increased serum bilirubin and high blood reticulocyte numbers.
Collectively, the genetic, hematologic, and pathologic data indicate a severe hematologic disorder caused by homozygosity for the fsn mutation that differs from other known hematologic mutations in the mouse. The mechanism whereby fsn induces the reported pleiotropic effects has yet to be elucidated.