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Blood, 15 March 2007, Vol. 109, No. 6, pp. 2389-2398.
Prepublished online as a Blood First Edition Paper on November 7, 2006; DOI 10.1182/blood-2006-02-003087.
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HEMATOPOIESIS
The transcription factors Scl and Lmo2 act together during development of the hemangioblast in zebrafish
Lucy J. Patterson1,
Martin Gering2,
Craig E. Eckfeldt3,
Anthony R. Green4,
Catherine M. Verfaillie3,
Stephen C. Ekker5, and
Roger Patient1
1 Weatherall Institute of Molecular Medicine, Oxford University, John Radcliffe Hospital, Headington, Oxford, United Kingdom;
2 Institute of Genetics, University of Nottingham, Queen's Medical Centre, Nottingham, United Kingdom;
3 Stem Cell Institute and Department of Medicine, University of Minnesota, Minneapolis;
4 Department of Haematology, Cambridge Institute for Medical Research, Cambridge University, United Kingdom;
5 Arnold and Mabel Beckman Center for Transposon Research, Department of Genetics, Cell Biology and Development, University of Minnesota, Minneapolis
The transcription factors Scl and Lmo2 are crucial for development of all blood. An important early requirement for Scl in endothelial development has also been revealed recently in zebrafish embryos, supporting previous findings in scl–/– embryoid bodies. Scl depletion culminates most notably in failure of dorsal aorta formation, potentially revealing a role in the formation of hemogenic endothelium. We now present evidence that the requirements for Lmo2 in zebrafish embryos are essentially the same as for Scl. The expression of important hematopoietic regulators is lost, reduced, or delayed, panendothelial gene expression is down-regulated, and aorta-specific marker expression is lost. The close similarity of the phenotypes for Scl and Lmo2 suggest that they perform these early functions in hemangioblast development within a multiprotein complex, as shown for erythropoiesis. Consistent with this, we find that scl morphants cannot be rescued by a non-Lmo2–binding form of Scl but can be rescued by non-DNA–binding forms, suggesting tethering to target genes through DNA-binding partners linked via Lmo2. Interestingly, unlike other hematopoietic regulators, the Scl/Lmo2 complex does not appear to autoregulate, as neither gene's expression is affected by depletion of the other. Thus, expression of these critical regulators is dependent on continued expression of upstream regulators, which may include cell-extrinsic signals.
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