Microcytic anemia in mk/mk mice is not corrected by retroviral- mediated gene transfer of wild-type p45 NF- E2.
Mice homozygous for the mk mutation have a severe hypochromic, microcytic anemia that is characterized by a decreased mean-corpuscular hemoglobin concentration and balanced alpha- and beta-globin-chain synthesis. Transplantation studies have shown that the defect in homozygous mk/mk mice is intrinsic to both the hematopoietic system and the gut. The gene for the hematopoietic-specific transcription factor, p45 NF- E2, has been found to cosegregate with the mk phenotype and contain a point mutation in mk/mk mice that results in an amino acid substitution (173V-->A). In order to test the hypothesis that this amino acid substitution is responsible for the mk phenotype, we have used recombinant retroviruses to introduce wild-type p45 NF- E2 into the bone marrow of mk/mk mice. Despite gene transfer and expression of p45 NF- E2 in erythroid cells, we found no evidence for correction of the phenotype in mk/mk mice. These results indicate that the mk mutation cannot be corrected by enforced expression of wild-type p45 NF- E2 and suggest that the 173V-->A mutation of the p45 NF- E2 gene is not the cause of anemia in mk/mk mice.[1]References
- Microcytic anemia in mk/mk mice is not corrected by retroviral-mediated gene transfer of wild-type p45 NF-E2. Ney, P.A., Farina, S.F., Bodine, D.M., Andrews, N.C., Orkin, S.H., Neinhuis, A.W. Exp. Hematol. (1995) [Pubmed]
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