Mevalonate Pathway-mediated ER Homeostasis Is Required for Haploid Stability in Human Somatic Cells

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  • Yaguchi Kan
    Graduate School of Life Science, Hokkaido University
  • Sato Kimino
    Graduate School of Life Science, Hokkaido University
  • Yoshizawa Koya
    Graduate School of Life Science, Hokkaido University
  • Mikami Daisuke
    Lipid Biofunction Section, Faculty of Advanced Life Science, Hokkaido University
  • Yuyama Kohei
    Lipid Biofunction Section, Faculty of Advanced Life Science, Hokkaido University
  • Igarashi Yasuyuki
    Lipid Biofunction Section, Faculty of Advanced Life Science, Hokkaido University
  • Banhegyi Gabor
    Institute of Biochemistry and Molecular Biology, Semmelweis University
  • Margittai Eva
    Institute of Translational Medicine, Semmelweis University
  • Uehara Ryota
    Graduate School of Life Science, Hokkaido University Faculty of Advanced Life Science, Hokkaido University

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<p>The somatic haploidy is unstable in diplontic animals, but cellular processes determining haploid stability remain elusive. Here, we found that inhibition of mevalonate pathway by pitavastatin, a widely used cholesterol-lowering drug, drastically destabilized the haploid state in HAP1 cells. Interestingly, cholesterol supplementation did not restore haploid stability in pitavastatin-treated cells, and cholesterol inhibitor U18666A did not phenocopy haploid destabilization. These results ruled out the involvement of cholesterol in haploid stability. Besides cholesterol perturbation, pitavastatin induced endoplasmic reticulum (ER) stress, the suppression of which by a chemical chaperon significantly restored haploid stability in pitavastatin-treated cells. Our data demonstrate the involvement of the mevalonate pathway in the stability of the haploid state in human somatic cells through managing ER stress, highlighting a novel link between ploidy and ER homeostatic control.</p><p>Key words: haploid, ER stress, Mevalonate pathway</p>

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