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 Blood, 1 March 2007, Vol. 109, No. 5, pp. 1908-1916.
Prepublished online as a Blood First Edition Paper on October 19, 2006; DOI 10.1182/blood-2006-05-023226.

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Submitted May 15, 2006
Accepted October 10, 2006

The paralogous haemopoietic regulators Lyl1 and SCL are co-regulated by Ets and GATA factors yet Lyl1 cannot rescue the early SCL-/- phenotype

Wan YI Chan, George A Follows, Georges Lacaud, John E Pimanda, Josette-Renee Landry, Sarah Kinston, Kathy Knezevic, Sandie Piltz, Ian J Donaldson, Laure Gambardella, Fred Sablitzky, Anthony R Green, Valerie Kouskoff, and Berthold Gottgens*

Cambridge Institute for Medical Research, University of Cambridge, United Kingdom
Christie Hospital, United Kingdom
University of Nottingham, United Kingdom

* Corresponding author; email: bg200{at}cam.ac.uk.

Transcription factors are key regulators of haematopoietic stem cells (HSCs) yet the molecular mechanisms that control their expression are largely unknown. Previously, we demonstrated that expression of SCL/TAL1, a transcription factor required for the specification of HSCs, is controlled by Ets and GATA factors. Here we characterise the molecular mechanisms controlling expression of Lyl1, a paralogue of SCL also required for HSC function. Two closely space promoters directed expression to haematopoietic progenitor, megakaryocytic and endothelial cells in transgenic mice. Conserved binding sites required for promoter activity were bound in vivo by GATA-2 and the Ets factors Fli1, Elf1, Erg and PU.1. However, despite coregulation of SCL and Lyl1 by the same Ets and GATA factors, SCL expression was initiated prior to Lyl1 in ES cell differentiation assays. Moreover, ectopic expression of SCL but not Lyl1 rescued haematopoietic differentiation in SCL-/- ES-cells thus providing a molecular explanation for the vastly different phenotypes of SCL-/- and Lyl1-/- mouse embryos. Furthermore, coregulation of SCL and Lyl1 later during development may explain the mild phenotype of SCL-/- adult HSCs.


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