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Papers In Press, published online ahead of print April 19, 2004
Department of Molecular Medicine, University of California, Torrance, CA 90502
Corresponding Author: lluou{at}ucla.edu
CTCF, a transcriptional regulator, plays important roles in epigenetics and development. In the present study, we report in transgenic mice that overexpression of CTCF during embryonic development suppresses the Pax6 gene expression. This effect causes defects in ocular development, which results in microophthalmia. In eye-derived cells transfected with a tetracycline turn-on CTCF system, up-regulation of CTCF expression significantly suppressed Pax6 expression. In contrast, the knockdown of CTCF mRNA resulted in the down-regulation of the CTCF protein expression, which in turn, enhanced the Pax6 expression. CTCF controls the Pax6 transcription by interacting with a repressor element located in the 5’-flanking region upstream of the Pax6 P0 promoter. This interaction suppressed the Pax6 gene transcription by blocking the effect of an ectoderm enhancer (EE) located 3.5 kb upstream from the P0 promoter. We also found an 80 bp sequence in a region –1.2 kbp upstream from the P0 promoter that contained multiple CTCF binding sites and interacted with nuclear proteins obtained from eye-derived cells forming EMSA complexes with CTCF. We conclude that a novel function of CTCF is to regulate the Pax6 transcription by binding to the repressor element, which in turn blocks the effect of EE resulting in the inhibition of P0 promoter activity.
J. Biol. Chem, 10.1074/jbc.M313942200
Submitted on December 19, 2003
Revised on March 29, 2004
Accepted on April 19, 2004
Regulation of eye development by transcription control of CTCF
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