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Transcription of the human colony-stimulating factor-1 receptor gene is
regulated by separate tissue-specific promoters
WM Roberts, LH Shapiro, RA Ashmun and AT Look
Department of Hematology-Oncology, St Jude Children's Research Hospital,
Memphis, TN 38105.
Receptors for macrophage colony-stimulating factor (CSF-1R) are expressed
not only by monocytes, macrophages, and their progenitors, but also by
placental trophoblasts during fetal development. In monocytes, CSF-1R gene
transcripts originate at multiple sites immediately upstream of the gene's
coding sequences, whereas in placental cells the transcripts include an
additional noncoding exon, located 26 kb upstream near the 3' end of the
B-type platelet-derived growth factor (PDGF) receptor gene. Physically
distinct CSF-1R transcription origins suggest separate promoter usage by
the two cell types. To identify regulatory elements of these promoters, we
fused CSF- 1R genomic sequences to bacterial reporter genes and introduced
the resulting constructs into human cell lines and mouse fibroblasts. A
775- bp genomic fragment containing CSF-1R placental transcription origins
and adjacent upstream sequences mediated reporter gene expression in BeWo
choriocarcinoma cells and mouse NIH-3T3 fibroblasts, but not in myeloid or
lymphoid cells. By contrast, a 550-bp genomic fragment containing CSF-1R
monocyte transcription origins and 5' flanking sequences directed gene
expression in U-937 human myeloid cells, but not in the other cell types.
Thus, nucleotide sequences of fewer than 1,000-bp upstream of the two
independent CSF-1R transcription origins contain the minimal promoter
elements needed to program appropriate tissue-specific expression of
reporter genes.
Volume 79,
Issue 3,
pp. 586-593,
02/01/1992
Copyright © 1992 by The American Society of Hematology
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