Transcriptional regulation of the mouse CSF-1 gene

Abstract

Research in our laboratory is aimed at understanding the cellular and molecular mechanisms that govern colony stimulating factor‐1 (CSF‐1) gene expression. Our hypothesis is that a basal set of trans‐acting factors is bound to the CSF‐1 gene during fibroblast proliferation, resulting in constitutive CSF‐1 gene expression. Modulation of CSF‐1 gene transcription by growth‐arrest (decrease) or stimulation of growth‐arrested fibroblasts (re‐initiate) is mediated by changes in the basal set of factors bound and/or by the addition of stimulus‐specific factors. We have extended our hypothesis to include other cell types (monocytes) to determine if mechanisms used to control CSF‐1 gene expression in fibroblasts are unique or represent common nontissue‐specific regulatory mechanisms. Analysis of CSF‐1‐CAT reporter constructs in transiently transfected fibroblasts and monocytes was used to identify CSF‐1 genomic sequences that affect transcriptional activity. DNase 1 protection, electrophoretic mobility shift, and methylation interference assays were used to identify the putative cis‐acting elements. Results of our study suggest multiple trans‐acting factors may regulate CSF‐1 gene expression; some may be tissue specific, while others, such as AP1, CTF/NF1, Spl, and Sp3, are shared in common. Mol Reprod Dev 46:39–45, 1997. © 1997 Wiley‐Liss, Inc.

Concerted Action of Smad and CREB-binding Protein Regulates Bone Morphogenetic Protein-2-stimulated Osteoblastic Colony-stimulating Factor-1 Expression

“…Our study is aimed at understanding the mechanism of CSF-1 gene regulation in osteoblast cells. Previous studies have shown that interleukin-1 and tumor necrosis factor are potent stimulators of CSF-1 gene expression (49). CSF-1 is released from osteoblasts constitutively and in response to parathyroid hormone and parathyroid hormonerelated protein (50).…”

Two Macrophage Colony-Stimulating Factor Genes Exist in Fish That Differ in Gene Organization and Are Differentially Expressed

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Tumor suppressor genes in normal and malignant hematopoiesis

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