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Erythroid Maturation and Globin Gene Expression in Mice With Combined
Deficiency of NF-E2 and Nrf-2
Florence Martin,
Jan M. van Deursen,
Ramesh A. Shivdasani,
Carl W. Jackson,
Amber G. Troutman, and
Paul A. Ney
From the Departments of Biochemistry, Genetics, and Experimental
Hematology, Saint Jude Children's Research Hospital, Memphis, TN; and
Dana-Farber Cancer Institute, Children's Hospital, Harvard Medical
School, Boston, MA.
NF-E2 binding sites, located in distant regulatory sequences, may be
important for high level  - and  -globin gene expression. Surprisingly, targeted disruption of each subunit of NF-E2 has either
little or no effect on erythroid maturation in mice. For p18 NF-E2,
this lack of effect is due, at least in part, to the presence of
redundant proteins. For p45 NF-E2, one possibility is that
NF-E2-related factors, Nrf-1 or Nrf-2, activate globin gene expression
in the absence of NF-E2. To test this hypothesis for Nrf-2, we
disrupted the Nrf-2 gene by homologous recombination. Nrf-2-deficient
mice had no detectable hematopoietic defect. In addition, no evidence
was found for reciprocal upregulation of NF-E2 or Nrf-2 protein in
fetal liver cells deficient for either factor. Fetal liver cells
deficient for both NF-E2 and Nrf-2 expressed normal levels of - and
-globin. Mature mice with combined deficiency of NF-E2 and Nrf-2 did
not exhibit a defect in erythroid maturation beyond that seen with loss
of NF-E2 alone. Thus, the presence of a mild erythroid defect in
NF-E2-deficient mice is not the result of compensation by Nrf-2.
Blood, Vol. 91 No. 9 (May 1), 1998:
pp. 3459-3466
© 1998 by The American Society of Hematology.
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