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Blood, Vol. 94 No. 11 (December 1), 1999:
pp. 3730-3736
Changes in Chromatin Organization at the Neutrophil Elastase Locus
Associated With Myeloid Cell Differentiation
Edmond T.L. Wong,
Dieter E. Jenne,
Michael Zimmer,
Susan D. Porter, and
C. Blake Gilks
From the Department of Pathology and Laboratory Medicine, University
of British Columbia, Vancouver, British Columbia, Canada; and the
Department of Neuroimmunology, Max-Planck Institute of Neurobiology,
the Department of Neuroimmunology, Planegg-Martinsried, Germany.
Neutrophil elastase, proteinase-3, and azurocidin are primary
components of neutrophil azurophilic granules and are encoded by
closely linked genes (gene symbols ELA2, PRTN3, and AZU1, respectively) in a region of approximately 50 kb. These genes are coordinately expressed in a granulocyte-specific fashion, but the mechanisms defining this pattern of expression are unknown. To understand the role
of chromatin organization in governing the expression of ELA2, PRTN3,
and AZU1, we mapped this region of chromosome 19 and identified the
adipsin (complement factor D) gene in proximity to the 3' end of ELA2.
We then examined the changes in chromatin structure at the locus which
accompany myeloid cell differentiation and identified 17 DNase I
hypersensitive sites (DHS 1 to 17) in U-937 cells, an early
myelomonocytic cell line expressing high levels of neutrophil elastase.
Chemically induced differentiation and concomitant downregulation of
AZU1, PRTN3, and ELA2 transcription in U-937 cells is not accompanied
by changes in the DHS-pattern. Mature neutrophils, however, do not
carry any of these hypersensitive sites, indicating a large degree of
chromatin remodeling at this locus accompanying terminal granulocytic
differentiation. Sixteen of the 17 DHS identified in U-937 cells are
also present in the HL-60 myelomonocytic cell line. Hematopoietic cell
lines representing the early erythroid and lymphocyte lineages, and a
nonhematopoietic cell line display a subset of the hypersensitive
sites. The altered chromatin structure specific to cells that actively
transcribe the AZU1-PRTN3-ELA2 genes suggests that chromatin
reorganization is an important mechanism regulating the
myeloid-specific transcription of this gene cluster.
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