An intrinsic but cell-nonautonomous defect in GATA-1-overexpressing mouse erythroid cells.

Journal article

GATA-1 is a tissue-specific transcription factor that is essential for the production of red blood cells. Here we show that overexpression of GATA-1 in erythroid cells inhibits their differentiation, leading to a lethal anaemia. Using chromosome-X-inactivation of a GATA-1 transgene and chimaeric animals, we show that this defect is intrinsic to erythroid cells, but nevertheless cell nonautonomous. Usually, cell nonautonomy is thought to reflect aberrant gene function in cells other than those...

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Authors: Whyatt, D; Lindeboom, F; Karis, A; Ferreira, R; Milot, E

• Journal: Nature
• Volume: 406
• Issue: 6795
• Pages: 519-524
• Publication date: 2000-08-01
• DOI: 10.1038/35020086
• EISSN: 1476-4687
• ISSN: 0028-0836
• Language: English
• Keywords: Dosage Compensation, Genetic; Erythroid Precursor Cells; Mice, Inbred C57BL; Anemia; Female; Crosses, Genetic; DNA-Binding Proteins; Apoptosis; Animals; Transcription Factors; Chimera; X Chromosome; Erythroid-Specific DNA-Binding Factors; Animals, Genetically Modified; GATA1 Transcription Factor; Mice; Erythropoiesis; Erythroblasts; Male; Signal Transduction