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E3, a hematopoietic-specific transcript directly regulated by the retinoic
acid receptor alpha
LM Scott, L Mueller and SJ Collins
Division of Molecular Medicine, Fred Hutchinson Cancer Research Center,
Seattle, WA 98104, USA.
Retinoic acid (RA)-induced maturation mediated by the retinoic acid
receptor alpha (RAR alpha) has been implicated in myeloid development. We
have used differential hybridization analysis of a cDNA library constructed
from the murine RA-inducible MPRO promyelocyte cell line to identify
immediate-early genes induced by RA during granulocytic differentiation.
E3, one of nine sequences identified, was upregulated in an immediate-early
manner, with transcript levels peaking after 60 minutes exposure to RA. E3
transcripts were RA-inducible in HL60 cells, but not in an RA-resistant
subclone, HL60R, that harbors a mutated RAR alpha gene. However, when HL60R
cells were transduced with a functional copy of the RAR alpha gene, RA
induced a 10-fold increase in E3 mRNA levels. E3 transcripts are present in
the myeloid, B-lymphoid, and erythroid lineages, absent in nonhematopoietic
cells, and encode a highly hydrophobic, potentially phosphorylated
polypeptide of unknown function with significant homology to a putative
protein expressed in myeloid cells. The murine E3 promoter harbors a single
bipartite retinoic acid response element which in transient transfection
assays conferred RA sensitivity. These results indicate that E3 is a
hematopoietic-specific gene that is an immediate target for the activated
RAR alpha during myelopoiesis.
Volume 88,
Issue 7,
pp. 2517-2530,
10/01/1996
Copyright © 1996 by The American Society of Hematology
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