Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

The AML1:CBFbeta transcription factor complex is essential for definitive hematopoiesis. Null mutations in mouse AML1 result in midgestational lethality with a complete lack of fetal liver hematopoiesis. While the cell autonomous nature and expression pattern of AML1 suggest an intrinsic role for this transcription factor in the developing hematopoietic system, no direct link to a functional cell type has been made. Here, we examine the consequences of AML1 loss in hematopoietic stem cells (HSC) of the mouse embryo. We demonstrate an absolute requirement for AML1 in functional HSCs. Moreover, haploinsufficiency results in a dramatic change in the temporal and spatial distribution of HSCs, leading to their early appearance in the normal position in the aorta-gonad-mesonephros region and also in the yolk sac.

Original publication




Journal article



Publication Date





423 - 431


Animals, Aorta, Cell Aggregation, Cell Differentiation, Colony-Forming Units Assay, Core Binding Factor Alpha 2 Subunit, DNA-Binding Proteins, Embryo Transfer, Embryo, Mammalian, Female, Gestational Age, Gonads, Haplotypes, Hematopoiesis, Hematopoietic Stem Cells, Male, Mesonephros, Mice, Mice, Inbred C57BL, Mice, Mutant Strains, Organ Culture Techniques, Proto-Oncogene Proteins, Transcription Factors, Yolk Sac