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Physiol. Genomics 11: 91-98, 2002. First published August 27, 2002; doi:10.1152/physiolgenomics.00112.2001
1094-8341/02 $5.00
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Received 3 December 2001; accepted in final form 9 August 2002.
Physiological Genomics 11:91-98 (2002)
1094-8341/02 $5.00 © 2002 American Physiological Society

Isolation and characterization of zebrafish NFE2

Stephen J. Pratt1,2,*, Anna Drejer2,*, Helen Foott1,2,*, Bruce Barut1,2, Alison Brownlie1,2, John Postlethwait5, Yasutake Kato6, Masayuki Yamamoto6 and Leonard I. Zon1,2

1 Howard Hughes Medical Institute, Boston, Massachusetts 02115
2 Children’s Hospital, Division of Hematology/Oncology, Boston, Massachusetts 02115
3 Dana-Farber Cancer Institute, Boston, Massachusetts 02115
4 Harvard Medical School, Boston, Massachusetts 02115
5 Institute of Neuroscience, University of Oregon, Eugene, Oregon 97403
6 Center for Tsukuba Advanced Research Alliance (TARA), University of Tsukuba, 1-1-1 Tennoudai, Tsukuba 305-8577, Japan

Vertebrate hematopoiesis is regulated by distinct cell-specific transcription factors such as GATA-1 and SCL. Mammalian p45-NFE2 was characterized for its ability to bind the hypersensitive sites of the globin locus control region. NFE2 is a member of a cap’n’collar (CNC) and basic zipper (BZIP) superfamily that regulates gene transcription. It has been implicated in diverse processes such as globin gene expression, oxidative stress, and platelet lineage differentiation. Here, we have isolated the zebrafish ortholog of NFE2. The gene is highly homologous, particularly in the DNA-binding domain. Mapping the zebrafish NFE2 to linkage group 23 establishes a region of chromosomal synteny with human chromosome 12, further suggesting evolutionary conservation. During embryogenesis, the zebrafish gene is expressed specifically in erythroid cells and also in the developing ear. NFE2 expression is lacking in zebrafish mutants that have no hematopoietic cells. An analysis of the sauternes mutant, which carries a mutation in the ALAS-2 gene and thus has defective heme synthesis, demonstrates higher levels of NFE2 expression than normal. This further establishes the block to erythroid differentiation in the sauternes mutant. Our studies demonstrate conservation of the vertebrate genetic program for the erythroid lineage.

hematopoiesis; transcription factors; erythroid lineage; sauternes mutant




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