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J. Biol. Chem., Vol. 277, Issue 38, 35156-35161, September 20, 2002
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From the To investigate the cellular role of dual
specificity Yak1-related kinase (Dyrk) 1, a nuclear localized dual
specificity protein kinase, we examined its effect on transcriptional
regulation using reporter gene assays. We found that Dyrk1 can
substantially enhance Gli1-dependent, but not
LEF-1-, c-Jun-, or Elk-dependent, gene transcription. In part, Dyrk1 does this through retaining Gli1 in the
nucleus. However, we also demonstrate that Dyrk1 can enhance the
transcriptional activity of Gli1-AHA, a nuclear export mutant, suggesting that Dyrk1 may be more directly involved in regulating the
transcriptional activity of Gli1. In addition, Dyrk1 acted synergistically with Sonic hedgehog (Shh) to induce gene
transcription and differentiation in mouse C3H10T1/2 cells. The
failure of Shh to stimulate Dyrk1 kinase activity suggests that Dyrk1
may not be directly regulated by the Shh signaling pathway but
functionally interacts with it. Thus, Gli1 transcriptional
activity may be subjected to further regulation in the cell nucleus by
a pathway distinct from Shh signaling, one mediated by Dyrk1.
Regulation of Gli1 Transcriptional Activity in the Nucleus
by Dyrk1*
§,,
,,¶¶
Department of Genetics and Developmental
Biology, University of Connecticut Health Center, Farmington,
Connecticut 06030, ¶ Karolinska Institutet, Department of
Bioscience and Center for Nutrition and Toxicology, Novum, SE-141
57 Huddinge, Sweden, National Institute of Chemical Physics and
Biophysics and Center of Gene Technology, Tallinn Technical University,
Tallinn, Estonia, ** Unidad de Neurobiologia del Desarrollo,
Instituto de Neurociencias, Universidad Miguel Hernandezy CSIC, Campus
de San Juan, 03550 Alicante, Spain, § Department of
Pharmacology, University of Rochester, Rochester, New York 14642, Department of Genetics, Southeast
University Medical School, Nanjing, China, and
§§ Department of Medicine/Genetic Medicine,
Vanderbilt University, Nashville, Tennessee 37232
*
This work was supported by grants from the National
Institutes of Health and American Cancer Society and by American Heart Association Established Investigator Award (to D. W.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
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