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 Blood, 15 February 2008, Vol. 111, No. 4, pp. 1946-1950.
Prepublished online as a Blood First Edition Paper on December 6, 2007; DOI 10.1182/blood-2007-04-085746.

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HEMATOPOIESIS

Brief Report

Hls5 regulated erythroid differentiation by modulating GATA-1 activity

Raelene Endersby1,2, Ian J. Majewski1,3, Louise Winteringham1, Jennifer G. Beaumont1, Amy Samuels1, Robin Scaife1, Esther Lim1, Merlin Crossley4, S. Peter Klinken1, and Jean-Philippe Lalonde1

1 Laboratory for Cancer Medicine, Western Australian Institute for Medical Research, Centre for Medical Research, University of Western Australia, Crawley, Australia; 2 Department of Developmental Neurobiology, St Jude Children's Research Hospital, Memphis, TN; 3 Division of Molecular Medicine, Walter and Eliza Hall Institute of Medical Research, Parkville, Australia; and 4 School of Molecular and Microbial Biosciences, University of Sydney, Sydney, Australia

Hemopoietic lineage switch (Hls) 5 and 7 were originally isolated as genes up-regulated during an erythroid-to-myeloid lineage switch. We have shown previously that Hls7/Mlf1 imposes a monoblastoid phenotype on erythroleukemic cells. Here we show that Hls5 impedes erythroid maturation by restricting proliferation and inhibiting hemoglobin synthesis; however, Hls5 does not influence the morphology of erythroid cells. Under the influence of GATA-1, Hls5 relocates from cytoplasmic granules to the nucleus where it associates with both FOG-1 and GATA-1. In the nucleus, Hls5 is able to suppress GATA-1–mediated transactivation and reduce GATA-1 binding to DNA. We conclude that Hls5 and Hls7/Mlf1 act cooperatively to induce biochemical and phenotypic changes associated with erythroid/myeloid lineage switching.


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