부산대학교 도서관

Mice with hemoglobin deficit (hbd) have a hypochromic, microcytic anemia inherited as an autosomal recessive. The mice also exhibit reticulocytosis, hyperferremia and elevated free protoporphyrin in red cells (Bannerman et al 1986 Proc Soc Exp Biol Med 182:52). The spontaneous mutation has been mapped to chromosome 19 (Bloom et al 1998 Mamm Genome 9:666), making it ripe for identification of the gene, given the power of mouse genetics. Until the actual locus is determined, however, some mice must be identified as +/? as dominant inheritance obscures the second allele. Prior studies established that hbd/hbdreticulocytes take up 125I-labelled transferrin as well as +/? controls, but are less effective at incorporating 59Fe from transferrin (Garrick et al 1987 Exp Hemato 15:671). Scatchard analysis showed the affinity of transferrin receptors for transferrin was similar in hbd/hbdversus +/? reticulocytes; slightly more receptors were present, however, on the surface of hbd/hbdreticulocytes.