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M J Dewey

Publications and source records attributed to M J Dewey.

60 records · Page 4Linked to original sources
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Genetic control of red cell osmotic fragility.

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 beta chain of hemoglobin (Hbb). Allelic differences at Fv-2, a gene known to control the proportion of erythroid 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 strans (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 strans 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.

Animals↗
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Genetic control of juvenile growth rate in mice: variation between a congenic strain and its background strain.

Studies on the genetic regulation of growth are confounded by the multigenic basis of growth. There is a need to isolate simplified genetic systems for the study of growth. We compared two closely related mouse strains and their F1 hybrids with regard to birth and weaning weights. The strains we used were C57BL/6 (B6) and a congenic derivative of B6 (HW54) that contains a short segment of BALB/c chromosome 7 spanning the H-24 and Gpi-1 loci. Despite the genetic similarity of these strains, they differed significantly in both birth and weaning weights. At birth, B6 pups were on average as much as 6.6% heavier than were pups from HW54. By the time of weaning, this trend was reversed; HW54 pups were as much as 13.8% heavier than were B6 pups. (B6 x HW54)F1 hybrids were intermediate between the parental strains in birth weight but were identical to B6 animals at weaning. An analysis of the F2 generation suggested that postnatal growth differences between B6 and HW54 are probably dependent on the maternal genotype. These strain-specific growth rates result from polymorphism at a restricted portion of the genome and represent a highly simplified system for the study of the genetics of growth.

Animals↗