Journal article

Shared roles for Scl and Lyl1 in murine platelet production and function

Sung K Chiu, Stephanie L Orive, Mitchell J Moon, Jesslyn Saw, Sarah Ellis, Benjamin T Kile, Yizhou Huang, Diego Chacon, John E Pimanda, Dominik Beck, Justin R Hamilton, Cedric S Tremblay, David J Curtis

Blood | AMER SOC HEMATOLOGY | Published : 2019

Abstract

The Stem Cell Leukemia (Scl or Tal1) protein forms part of a multimeric transcription factor complex required for normal megakaryopoiesis. However, unlike other members of this complex such as Gata1, Fli1 and Runx1, mutations of Scl have not been observed as a cause of inherited thrombocytopenia. We postulated that functional redundancy with its closely related family member, Lymphoblastic Leukemia 1 (Lyl1) might explain this observation. To determine if Lyl1 can substitute for Scl in megakaryopoiesis, we examined the platelet phenotype of mice lacking one or both factors in megakaryocytes. Conditional Scl knockout mice crossed with transgenic mice expressing Cre recombinase under the contro..

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Grants

Awarded by Australian National Health and Medical Research Council (NHMRC)


Funding Acknowledgements

This work was supported by a project grant (APP1052313) (D.J.C.) from the Australian National Health and Medical Research Council (NHMRC), a Leukaemia Foundation scholarship (S.K.C.), a Senior Medical Research Fellowship from the Sylvia and Charles Viertel Foundation (D.J.C.), a Cancer Institute University of New South Wales Fellowship (D.B.), and by funding from the NHMRC, Anthony Rothe Foundation (J.E.P.), Cancer Australia (D.B.), Gilead Sciences (D.B.) and anNHMRC Peter Doherty fellowship (D.B.).