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 Blood, 1 October 2008, Vol. 112, No. 7, pp. 2722-2729.
Prepublished online as a Blood First Edition Paper on July 14, 2008; DOI 10.1182/blood-2008-02-140806.

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HEMATOPOIESIS AND STEM CELLS

Lymphoid-affiliated genes are associated with active histone modifications in human hematopoietic stem cells

Jerome Maës1,2,*, Marta Maleszewska1,2,*, Claire Guillemin3,4, Francoise Pflumio3,4, Emmanuelle Six5,6, Isabelle André-Schmutz5,6, Marina Cavazzana-Calvo5,6, Dominique Charron1,2, Claire Francastel3,4, and Michele Goodhardt1,2

1 Institut Universitaire d'Hématologie, Université Paris 7 Denis Diderot, Paris; 2 Inserm U662, Paris; 3 Institut Cochin, Université Paris Descartes, CNRS (UMR 8104), Paris; 4 Inserm U567, Paris; 5 Inserm U768, Paris; and 6 Université Paris-Descartes, Faculté de Médecine René Descartes, Paris, France

To address the role of chromatin structure in the establishment of hematopoietic stem cell (HSC) multilineage potential and commitment to the lymphoid lineage, we have analyzed histone modifications at a panel of lymphoid- and myeloid-affiliated genes in multipotent and lineage-committed hematopoietic cells isolated from human cord blood. Our results show that many B- and T-lymphoid genes, although silent in HSCs, are associated with acetylated histones H3 and H4. We also detected histone H3 lysine 4 methylation but not repressive lysine 9 or 27 methylation marks at these loci, indicative of an open chromatin structure. Interestingly, the relative level of H3 lysine 4 dimethylation to trimethylation at B-specific loci was high in multipotent CD34+CD38lo progenitors and decreased as they become actively transcribed in B-lineage cells. In vitro differentiation of CD34+ cells toward the erythroid, granulocyte, and T-cell lineages resulted in a loss of histone acetylation at nonlineage-associated genes. This study provides evidence that histone modifications involved in chromatin decondensation are already in place at lymphoid-specific genes in primary human HSCs, supporting the idea that these genes are "primed" for expression before lineage commitment. This permissive chromatin structure is progressively lost as the stem cell differentiates.


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