Characteristics of the CFU-s population in mice carrying the Slj allele.

A tentative characterization of haemopoietic stem cells with respect to their organ distribution, seeding fraction and colony formation in the spleen, radiosensitivity and humoral regulation was attempted in mice heterozygous for the mutant allele Slj and in their normal littermates. Slj/+ mice were characterized by a deficient CFU-s content of the blood and spleen and had slightly lower femoral CFU-s numbers. This CFU-s distribution could not be explained by differences in seeding efficiency 'f' between CFU-s of Slj/+ and +/+ origin in lethally irradiated recipients used in the CFU-s assay. The seeding fraction of CFU-s of +/+ origin did not differ in +/+ and Slj/+ recipients. However, in irradiated Slj/+ recipient mice a 30% decrease was observed in the number of the colonies derived from splenic and femoral CFU-s of both +/+ and Slj/+ origin. The serum level of SHSF (splenic haemopoiesis stimulating factor) was decreased in Slj/+ mice, but significantly increased in Sl/Sld mice, as compared to their respective normal +/+ littermates. Endogenous colony formation in Slj/+ spleens was deficient in comparison to that observed in +/+ spleens, and distinct sex differences were observed. However, mutant and normal CFU-s from spleen and bone marrow had a similar survival following in-vitro gamma irradiation. Femurs and spleens of both Slj/+ and +/+ origin were implanted into both Slj/+ and +/+ hosts. Six weeks later the Slj/+ grafts contained less CFU-s than the +/+ grafts. These data show that the splenic stroma of Slj/+ mice is not defective in its capacity to lodge injected CFU-s but is deficient in its ability to maintain CFU-s under 'steady-state' conditions and stimulate their colony formation in a 'perturbed state'. Some of the characteristics of Slj/+ mice segregate them from Sl/Sld mice, i.e. a deficient splenic CFU-s content, normal seeding fractions 'f' of CFU-s from spleen and bone marrow in the presence of an almost compensated anemia, and decreased serum levels of SHSF. The study of the Slj trait may be a useful extension of the current Sl/Sld model for exploration of hereditary defects in haematopoietic stroma.