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Papers In Press, published online ahead of print July 25, 2001
INSERM U489, 75020, Paris Cedex 20
Corresponding Author: jerome.rossert{at}tnn.ap-hop-paris.fr
The transcription of type I collagen genes is tightly regulated, but few cis-acting elements have been identified that can modulate the levels of expression of these genes. Generation of transgenic mice harboring various segments of the mouse pro-alpha1(I) collagen promoter led us to suspect that a repressor element was located between -10.5 kb and -17 kb. Stable and transient transfection experiments in ROS17/2.8 osteoblastic cells confirmed the existence of such a repressor element at about -14 kb, and showed that it consists in an almost perfect three-time repeat of a 41-bp sequence. This element, that we named COIN-1, contains three E2 boxes, and a point mutation in at least two of them completely abolished its repressor effect. In gel shift assays, COIN-1 bound a DNA-binding protein named deltaEF1, and mutations that abolished the repressor effect of COIN-1 also suppressed the binding of deltaEF1. We also showed that the repressor effect of COIN-1 was not mediated by chromatin compaction. Furthermore, overexpression of deltaEF1 in ROS17/2.8 osteoblastic cells enhanced the inhibitory effect of COIN-1 in a dose-dependent manner, and repressed the expression of the pro-alpha1(I) collagen gene. Thus, deltaEF1 appears to repress the expression of the mouse pro-alpha1(I) collagen gene, through its binding to COIN-1.
J. Biol. Chem, 10.1074/jbc.M104185200
Submitted on May 9, 2001
Revised on June 27, 2001
Accepted on July 24, 2001
EF1 binds to a far-upstream sequence of the pro 
1(I) collagen gene and represses its expression in osteoblasts
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