MLX Is a Transcriptional Repressor of the Mammalian Golgi Stress Response

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  • Taniguchi Mai
    Department of Molecular Biochemistry, Graduate School of Life Science, University of Hyogo
  • Sasaki-Osugi Kanae
    Department of Molecular Biochemistry, Graduate School of Life Science, University of Hyogo
  • Oku Masaya
    Department of Biophysics, Graduate School of Science, Kyoto University
  • Sawaguchi Shogo
    Department of Molecular Biochemistry, Graduate School of Life Science, University of Hyogo
  • Tanakura Soichiro
    Department of Molecular Biochemistry, Graduate School of Life Science, University of Hyogo
  • Kawai Yumeto
    Department of Molecular Biochemistry, Graduate School of Life Science, University of Hyogo
  • Wakabayashi Sadao
    Department of Molecular Biochemistry, Graduate School of Life Science, University of Hyogo
  • Yoshida Hiderou
    Department of Molecular Biochemistry, Graduate School of Life Science, University of Hyogo Department of Biophysics, Graduate School of Science, Kyoto University

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Abstract

<p>The Golgi stress response is a homeostatic mechanism that controls the capacity of the Golgi apparatus in accordance with cellular demands. When the capacity of the Golgi apparatus becomes insufficient (Golgi stress), transcription levels of Golgi-related genes encoding glycosylation enzymes, a Golgi structural protein, and components of vesicular transport are upregulated through a common cis-acting enhancer—the Golgi apparatus stress response element (GASE). Here, we identified the transcription factor MLX as a GASE-binding protein. MLX resides in the cytoplasm and does not bind to GASE in normal growth conditions, whereas MLX translocates into the nucleus and specifically binds to GASE in response to Golgi stress. Suppression of MLX expression increased transcriptional induction of target genes of the Golgi stress response, whereas overexpression of MLX reduced GASE-binding of TFE3 as well as transcriptional induction from GASE, suggesting that MLX is a transcriptional repressor of the mammalian Golgi stress response.</p>

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