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The Journal of Heredity 1985:76(1):31-35
© 1985 The American Genetic Association 76:31-35

research-article

Genetic control of red cell osmotic fragility

N. Kathleen Norman, and Michael J. Dewey

The authors are affiliated with the Department of Biology, University of South Carolina, Columbia, SC 29208. This research was supported in part by grants from the Research and Productive Scholarship Fund of the University of South Carolina and from the American Cancer Society (MV105A). The authors are grateful to Drs. M. R. Felder and W. D. Dawson for critical reading of the manuscript and to Ms. B. Branham for help in its preparation. Please address reprint requests to Dr. Dewey.

Abstract

Among normal mouse strains, natural genetic variation offers the potential to investigate the structure and function of cell membranes. One such polymorphism between C57BL/6J and DBA/2J is a difference in erythrocyte sensitivity to osmotic lysis. The genetic basis for erythrocyte osmotic fragility differences between mouse strains C57BL/6 and DBA/2 was examined through analyses of their serial backcross progeny, recombinant inbred (RI) strains (BXD), and congenic C57BL/6 strains with allelic differences at Hbb or Fv-2. The data indicate that the fragility difference between C57BL/6 and DBA/2 is the result of allelic differences at a minimum of two segregating loci. One of these might be linked to, but is not identical with the gene encoding the ß chain of hemoglobin (Hbb). Allelic differences at Fv-2, a gene known to control the proportion of erythrold precursors in the S phase, and at Hba, the structural locus of hemoglobin {alpha} chain also appear to exert no major influence on red cell osmotic fragility. Furthermore, the fact that red cells from one of the RI strains (BXD-31) are strikingly more resistant than those from the resistant parental strain DBA/2 leads to the conclusion that the degree of resistance/susceptibility for either strain is determined by the combined contributions of gene effects not all of which act in the same direction. We also found that red cells from strains C57BL/6 and DBA/2 differ in their uptake of 51Cr. This result suggests the possibility that red cell osmotic fragility differences may be due in part to differences in ion metabolism or membrane transport.


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