c-Jun and Sp1 family are critical for retinoic acid induction of the lamin A/C retinoic acid-responsive element

Biochemical and Biophysical Research Communications
Koichi OkumuraNoboru Nakajima

Abstract

The expression of A-type lamins, subdivided into lamin A and C, is developmentally regulated. Retinoic acid (RA)-induced differentiation of P19 embryonic carcinoma cells, in which A-type lamins are absent, increases the expression of lamin A/C. We previously showed, using P19 cells as a model system, that the lamin A/C promoter has a retinoic acid-responsive element (L-RARE), and that Sp1 and Sp3 bind the CACCC box of the L-RARE. In this study, we report that Sp1, Sp3, and c-Jun increase transactivation of the L-RARE during RA treatment. Sp1 and Sp3 regulate the lamin A/C promoter in Sp1-deficient SL2 cells and contribute to RA-dependent activation in GAL4-based transcriptional assays. Overexpression of c-Jun causes transactivation of a chimeric promoter consisting of four tandem L-RARE repeats fused with the luciferase gene in P19 cells. c-Jun also transactivates a reporter construct with five tandem GAL4-binding sites, only when co-expressed with either GAL4-Sp1 or Sp3 fusion proteins. Furthermore, we detect a physiological interaction between c-Jun with Sp1/Sp3 in RA-treated cells. Our data suggest that Sp1, Sp3, and c-Jun play an important role in gene expression through the L-RARE during RA treatment.

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Citations

Feb 23, 2013·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Jessika BertacchiniSandra Marmiroli
Jun 28, 2016·The Journal of Immunology : Official Journal of the American Association of Immunologists·Krishnakumar MaluPeter Gaines
May 17, 2005·Journal of Cellular Physiology·Jae H LimJustin R Fallon
Jul 12, 2016·European Journal of Cell Biology·Emily S Bell, Jan Lammerding
Jun 26, 2014·Journal of Cell Science·Joe Swift, Dennis E Discher

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