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Miz1 is required to maintain autophagic flux

Author

Listed:
  • Elmar Wolf

    (Theodor Boveri Institute, Biocenter, University of Würzburg, Am Hubland, 97074 Würzburg, Germany)

  • Anneli Gebhardt

    (Theodor Boveri Institute, Biocenter, University of Würzburg, Am Hubland, 97074 Würzburg, Germany)

  • Daisuke Kawauchi

    (MS#350, Danny Thomas Research Center, 5006C, St. Jude Children’s Research Hospital)

  • Susanne Walz

    (Theodor Boveri Institute, Biocenter, University of Würzburg, Am Hubland, 97074 Würzburg, Germany)

  • Björn von Eyss

    (Theodor Boveri Institute, Biocenter, University of Würzburg, Am Hubland, 97074 Würzburg, Germany)

  • Nicole Wagner

    (Institute for Anatomy and Cell Biology, University of Würzburg, Koellikerstrasse 6, 97070 Würzburg, Germany)

  • Christoph Renninger

    (Institute for Anatomy and Cell Biology, University of Würzburg, Koellikerstrasse 6, 97070 Würzburg, Germany)

  • Georg Krohne

    (Theodor Boveri Institute, Biocenter, University of Würzburg, Am Hubland, 97074 Würzburg, Germany)

  • Esther Asan

    (Institute for Anatomy and Cell Biology, University of Würzburg, Koellikerstrasse 6, 97070 Würzburg, Germany)

  • Martine F. Roussel

    (MS#350, Danny Thomas Research Center, 5006C, St. Jude Children’s Research Hospital)

  • Martin Eilers

    (Theodor Boveri Institute, Biocenter, University of Würzburg, Am Hubland, 97074 Würzburg, Germany
    Comprehensive Cancer Center Mainfranken, Josef-Schneider-Strasse 6, 97080 Würzburg, Germany)

Abstract

Miz1 is a zinc finger protein that regulates the expression of cell cycle inhibitors as part of a complex with Myc. Cell cycle-independent functions of Miz1 are poorly understood. Here we use a Nestin-Cre transgene to delete an essential domain of Miz1 in the central nervous system (Miz1ΔPOZNes). Miz1ΔPOZNes mice display cerebellar neurodegeneration characterized by the progressive loss of Purkinje cells. Chromatin immunoprecipitation sequencing and biochemical analyses show that Miz1 activates transcription upon binding to a non-palindromic sequence present in core promoters. Target genes of Miz1 encode regulators of autophagy and proteins involved in vesicular transport that are required for autophagy. Miz1ΔPOZ neuronal progenitors and fibroblasts show reduced autophagic flux. Consistently, polyubiquitinated proteins and p62/Sqtm1 accumulate in the cerebella of Miz1ΔPOZNes mice, characteristic features of defective autophagy. Our data suggest that Miz1 may link cell growth and ribosome biogenesis to the transcriptional regulation of vesicular transport and autophagy.

Suggested Citation

  • Elmar Wolf & Anneli Gebhardt & Daisuke Kawauchi & Susanne Walz & Björn von Eyss & Nicole Wagner & Christoph Renninger & Georg Krohne & Esther Asan & Martine F. Roussel & Martin Eilers, 2013. "Miz1 is required to maintain autophagic flux," Nature Communications, Nature, vol. 4(1), pages 1-12, December.
    • Handle: RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms3535
    DOI: 10.1038/ncomms3535
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    1. Quetzalcoatl Escalante-Covarrubias & Lucía Mendoza-Viveros & Mirna González-Suárez & Román Sitten-Olea & Laura A. Velázquez-Villegas & Fernando Becerril-Pérez & Ignacio Pacheco-Bernal & Erick Carreño-, 2023. "Time-of-day defines NAD+ efficacy to treat diet-induced metabolic disease by synchronizing the hepatic clock in mice," Nature Communications, Nature, vol. 14(1), pages 1-24, December.

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