PMID:7830794

Citation	Shivdasani, RA, Mayer, EL and Orkin, SH (1995) Absence of blood formation in mice lacking the T-cell leukaemia oncoprotein tal-1/SCL. Nature 373:432-4
Abstract	Chromosomal translocations associated with malignancies often result in deregulated expression of genes encoding transcription factors. In human T-cell leukaemias such regulators belong to diverse protein families and may normally be expressed widely (for example, Ttg-1/rbtn1, Ttg-2/rbtn2), exclusively outside the haematopoietic system (for example, Hox11), or specifically in haematopoietic cells and other selected sites (for example, tal-1/SCL, lyl-1). Aberrant expression within T cells is though to interfere with programmes of normal maturation. The most frequently activated gene in acute T-cell leukaemias, tal-1 (also called SCL), encodes a candidate regulator of haematopoietic development, a basic-helix-loop-helix protein, related to critical myogenic and neurogenic factors. Here we show by targeted gene disruption in mice that tal-1 is essential for embryonic blood formation in vivo. With respect to embryonic erythropoiesis, tal-1 deficiency resembles loss of the erythroid transcription factor GATA-1 or the LIM protein rbtn2. Profound reduction in myeloid cells cultured in vivo from tal-1 null yolk sacs suggests a broader defect manifest at the myelo-erythroid or multipotential progenitor cell level.
Links	PubMed Online version:10.1038/373432a0
Keywords	Animals; Base Sequence; Basic Helix-Loop-Helix Transcription Factors; DNA Primers; DNA-Binding Proteins/genetics; DNA-Binding Proteins/physiology; Erythropoiesis/physiology; Fetal Blood; Mice; Mice, Inbred C57BL; Molecular Sequence Data; Proto-Oncogene Proteins; T-Lymphocytes; Transcription Factors
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Annotations

Gene product	Qualifier	GO Term	Evidence Code	with/from	Aspect	Extension	Notes	Status
MOUSE:TAL1	acts_upstream_of_or_within	GO:0035162: embryonic hemopoiesis	ECO:0000315: mutant phenotype evidence used in manual assertion	MGI:MGI:1857254	P		Seeded From UniProt	complete

References

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