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Nucleic Acids Research Advance Access published online on February 20, 2009
Nucleic Acids Research, doi:10.1093/nar/gkp083
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© 2009 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Gene Regulation, Chromatin, and Epigenetics

The ubiquitously expressed bZIP inhibitor, JDP2, suppresses the transcription of its homologue immediate early gene counterpart, ATF3

Keren Weidenfeld-Baranboim1, Tal Hasin1, Ilona Darlyuk1, Ronit Heinrich1, Ofer Elhanani1, Jianzhi Pan2, Kazunari K. Yokoyama3,4 and Ami Aronheim1,*

1Department of Molecular Genetics, The Rappaport Family Institute for Research in the Medical Sciences, Technion-Israel Institute of Technology, Haifa 31096, Israel, 2Gene Engineering Division, Department of Biological Systems, BioResource Center, RIKEN, Tsukuba Science City, Ibaraki 305-0074, 3Gene Engineering Division, RIKEN BioResource Center, Tsukuba Science City, Ibaraki 305-0074, Japan and 4Graduate School of Medicine, Center of Excellence of Environmental Medicine, Kaohsiung Medical University, 807 Kaohsiung City, Taiwan

*To whom correspondence should be addressed. Tel: +972 4 829 5226; Fax: +972 4 829 5225; Email: aronheim{at}tx.technion.ac.il

Received December 8, 2008. Revised January 29, 2009. Accepted January 29, 2009.

JDP2 is a ubiquitously expressed bZIP repressor protein. JDP2 binds TPA response element and cyclic AMP response element located within various promoters. JDP2 displays a high degree of homology to the immediate early gene ATF3. ATF3 plays a crucial role in the cellular adaptive response to multiple stress insults as well as growth stimuli. We have identified ATF3 as a potential target gene for JDP2 repression. JDP2 regulates the ATF3 promoter potentially through binding to both the consensus ATF/CRE site and a non-consensus ATF3 auto-repression DNA-binding element. Expression of ATF3 protein in wild-type mouse embryo fibroblast (MEF) cells is below the detectable levels, whereas, JDP2 disrupted MEF cells display noticeable level of ATF3 protein. Following either serum or ER stress stimulation, ATF3 expression is potentiated in JDP2-KO fibroblast cells as compared with wild-type cells. Mice with either JDP2 over-expression or JDP2 disruption display undetectable level of ATF3 protein. However, ATF3 induction in response to either growth or stress signals is dependent on JDP2 expression level. ATF3 induction is attenuated in JDP2 over-expressing mice whereas is potentiated in JDP2-KO mice as compared with the corresponding wild-type mice. Collectively, the data presented strongly suggest that JDP2 plays a role in the determination of the ATF3 adaptive cellular threshold response to different stress insults and growth stimuli.


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