Characterization and genetic studies of microcytic anemia in house mouse.

H EREDITARY ANEMIAS in the mouse attract interest because of their pertinence for increased understanding of the etiology of variations in morphology and function of erythroid tissues and because of their potential value for studies of gene action in mammals. A number of different mutants affecting fetal or adult hemopoiesis, or both, have been reported.’3 A recent addition to this repertoire is microcytic anemia ( mk/mk), “inherited as an autosomal recessive with 100 per cent penetrance . . . as regards the anemic condition,” which involves “a compensatory increase in the production of red blood cells . . . approximately one-half normal size . . . so that by weaning age” ink! mk mice have more erythrocytes per unit blood volume than do their normal sibs.4 Since 1964 we have’ placed the mk mutant gene on three different homogeneous genetic backgrounds, and attempted to place it on a fourth; (2) tested for and eliminated allelism of the mk mutant with two other recessive mutant genes, ja and ha, responsible for hemolytic anemias; ( 3 ) characterized the anemia more fully by establishing typical blood values for mk/mk ( versus congenic mk/ + and + I + young adults ) ; (4) identified mk/mk vs. mk/ + fetuses in segregating litters; ( 5 ) followed the growing erythron of mk/mk and littermate normal mice from birth through 60 days; (6) analyzed the osmotic fragility of mk/mk erythrocytes; and ( 7) proved by genetic means that this particular anemia does not result from alteration of either the a-chain or the fl-chain of adult hemoglobin. The present paper reports results of these studies.