Lethal beta-thalassaemia in mice lacking the erythroid CACCC-transcription factor EKLF

Article Abstract:

Erythyroid Kruppel-like factor- (EKLF) deficient mice were created via gene targeting to determine EKLF's function in vivo. The embryos, which succumb to anemia during erythropoiesis of the fetal liver, were found to possess the molecular and hematological features of beta-globin deficiency, which is found in beta-thalassemia. Yolk sac erythropoiesis, erythroid commitment or the expression of other potential target genes do not require EKLF even if it is expressed at all stages. The stage-specific and beta-globin-gene specific requirements hint at the ability of EKLF to make the fetal-to-adult switch easier in humans.

Anemia, Nucleotides, Globin genes, Thalassemia

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Defective haematopoiesis in fetal liver resulting from inactivation of the EKLF gene

Article Abstract:

The erythroid Kruppel-like factor (EKLF) gene was inactivated by inserting a lacZ reporter gene via homologous recombination in embryonic stem cells. An analysis of the heterozygous EKLF+/- mice used in the experiment shows the reporter gene to be expressed in a developmentally specific way for all the different erythroblasts in the fetal liver and adult bone marrow. The homozygous EKLF+/- mice seem normal during the embryonic stage of hematopoiesis in the yolk sac. However, these mice were found to develop a deadly anemia in the early fetal stages when hematopoiesis had shifted to the liver.

Liver, Hematopoiesis

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Absence of blood formation in mice lacking the T-cell leukaemia oncoprotein tal-1/SCL

Article Abstract:

Examination of mice, which lack the T-cell leukaemia oncoprotein tal-1/SCL, generated by targeted gene disruption, indicates that in vivo embryonic blood formation requires tal-1. Embryonic erythropoiesis due to tal-1 deficiency is similar to that due to the loss of the erythroid transcription factor GATA-1 or the LIM protein rbtn2. Reverse transcriptase-polymerase chain reaction analysis of RNA derived from tal-1 null yolk sacs reveals significant decrease in myeloid cells, indicating the influence of tal-1 deficiency on multipotential progenitor cell level or myelo-erythroid.

Mice, mutant strains, Mutant mice

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