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

摘要: GATA-1 is a tissue-specific transcription factor that essential for the production of red blood cells. Here we show overexpression in erythroid cells inhibits their differentiation, leading to lethal anaemia. Using chromosome-X-inactivation transgene and chimaeric animals, this defect intrinsic cells, but nevertheless cell nonautonomous. Usually, nonautonomy thought reflect aberrant gene function other than those exhibit phenotype. On basis our data, propose an alternative mechanism which signal originating from wild-type restores normal differentiation overexpressing vivo. The existence such signalling indicates previous interpretations cell-nonautonomous defects may be erroneous some cases fact assign incorrect types.