1: Curr Biol. 2001 Sep 4;11(17):1353-7. 

Critical role of biklf in erythroid cell differentiation in zebrafish.

Kawahara A, Dawid IB.

Laboratory of Molecular Genetics, National Institute of Child Health and Human
Development, National Institutes of Health, Bethesda, MD 20892, USA.

Hematopoietic cells arise from ventral mesoderm in different vertebrates, but
the mechanisms through which various factors contribute to the hematopoietic
processes, including erythrogenesis, remain incompletely understood. The
Kruppel-like transcription factor Biklf is preferentially expressed in blood
islands throughout zebrafish embryogenesis, marking the region of future
erythropoiesis [1]. In this paper, we show that expression of biklf is
significantly suppressed in the blood-less mutants vampire and m683 in which
primitive hematopoiesis is impaired. Knockdown of biklf using morpholino-based
antisense oligonucleotides (biklf-MO) led to a potent reduction in the number of
circulating blood cells and deficiency in hemoglobin production. Consistently,
we found that the expression of beta(e3)globin is strongly suppressed in
biklf-MO-injected embryos, while gata1 expression is partly inhibited at the
10-somite stage. In addition, analysis of reporter constructs driven by the
GATA1 and beta-globin promoters showed that Biklf can positively regulate both
genes. These results indicate that Biklf is required for erythroid cell
differentiation in zebrafish.

PMID: 11553329 [PubMed - indexed for MEDLINE]


---------------------------------------------------------------