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The 19S proteasomal lid subunit POH1 enhances the transcriptional activation by Mitf in osteoclasts

Authors

  • Toni Schwarz,

    1. Department of Developmental and Surgical Science, University of Minnesota School of Dentistry, 515 Delaware St SE, Minneapolis, Minnesota 55455
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  • Chee Sohn,

    1. Department of Developmental and Surgical Science, University of Minnesota School of Dentistry, 515 Delaware St SE, Minneapolis, Minnesota 55455
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  • Bria Kaiser,

    1. Department of Developmental and Surgical Science, University of Minnesota School of Dentistry, 515 Delaware St SE, Minneapolis, Minnesota 55455
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  • Eric D. Jensen,

    1. Department of Diagnostic and Biological Sciences, University of Minnesota School of Dentistry, 515 Delaware St SE, Minneapolis, Minnesota 55455
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  • Kim C. Mansky

    Corresponding author
    1. Department of Developmental and Surgical Science, University of Minnesota School of Dentistry, 515 Delaware St SE, Minneapolis, Minnesota 55455
    • Department of Developmental and Surgical Science, University of Minnesota School of Dentistry, 6-320 Moos Tower, 515 Delaware St SE, Minneapolis MN 55455.
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Abstract

The microphthalmia-associated transcription factor (Mitf) regulates gene expression required for osteoclast differentiation. Genes regulated by Mitf have been previously identified. However, proteins that interact and regulate Mitf's activity in osteoclasts are not well known. Here, we report that POH1, a subunit of the 19S proteasome lid is a regulator of Mitf. We show that POH1 and Mitf interact in osteoclasts and that this interaction is dependent on RANKL signaling. Overexpression of POH1 increased Mitf's activation of 5XGal4-TK and Acp5 promoters. The amino terminus of POH1 mediates the binding to Mitf and is sufficient to increase Mitf's transcriptional activity. Finally, we show that mutations in the JAMM motif of POH1 reduced Mitf activation of promoters. In summary, our results identify a novel mechanism of Mitf regulation in osteoclasts by POH1. J. Cell. Biochem. 109: 967–974, 2010. © 2010 Wiley-Liss, Inc.

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