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  • 1.
    Li, Shuijie
    et al.
    Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden; College of Pharmacy, Harbin Medical University, Harbin, China.
    Li, Wenyu
    Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
    Yuan, Juan
    Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
    Bullova, Petra
    Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
    Wu, Jieyu
    Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
    Zhang, Xuepei
    Department of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden.
    Liu, Yong
    Department of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden.
    Plescher, Monika
    Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
    Rodriguez, Javier
    Edinburgh Cancer Research Centre, IGMM, University of Edinburgh, Edinburgh, United Kingdom.
    Bedoya-Reina, Oscar C.
    Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
    Jannig, Paulo R.
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Valente-Silva, Paula
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Yu, Meng
    Department of Medicine, Karolinska University Hospital, Stockholm, Sweden.
    Henriksson, Marie Arsenian
    Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
    Zubarev, Roman A.
    Department of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden.
    Smed-Sörensen, Anna
    Department of Medicine, Karolinska University Hospital, Stockholm, Sweden.
    Suzuki, Carolyn K.
    Department of Microbiology, Biochemistry and Molecular Genetics, Rutgers University-New Jersey Medical School, NJ, Newark, United States.
    Ruas, Jorge L.
    Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
    Holmberg, Johan
    Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten).
    Larsson, Catharina
    Department of Oncology-Pathology, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
    Christofer Juhlin, C.
    Department of Oncology-Pathology, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
    von Kriegsheim, Alex
    Edinburgh Cancer Research Centre, IGMM, University of Edinburgh, Edinburgh, United Kingdom.
    Cao, Yihai
    Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
    Schlisio, Susanne
    Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
    Impaired oxygen-sensitive regulation of mitochondrial biogenesis within the von Hippel–Lindau syndrome2022Ingår i: Nature Metabolism, E-ISSN 2522-5812, Vol. 4, nr 6, s. 739-758Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Mitochondria are the main consumers of oxygen within the cell. How mitochondria sense oxygen levels remains unknown. Here we show an oxygen-sensitive regulation of TFAM, an activator of mitochondrial transcription and replication, whose alteration is linked to tumours arising in the von Hippel–Lindau syndrome. TFAM is hydroxylated by EGLN3 and subsequently bound by the von Hippel–Lindau tumour-suppressor protein, which stabilizes TFAM by preventing mitochondrial proteolysis. Cells lacking wild-type VHL or in which EGLN3 is inactivated have reduced mitochondrial mass. Tumorigenic VHL variants leading to different clinical manifestations fail to bind hydroxylated TFAM. In contrast, cells harbouring the Chuvash polycythaemia VHLR200W mutation, involved in hypoxia-sensing disorders without tumour development, are capable of binding hydroxylated TFAM. Accordingly, VHL-related tumours, such as pheochromocytoma and renal cell carcinoma cells, display low mitochondrial content, suggesting that impaired mitochondrial biogenesis is linked to VHL tumorigenesis. Finally, inhibiting proteolysis by targeting LONP1 increases mitochondrial content in VHL-deficient cells and sensitizes therapy-resistant tumours to sorafenib treatment. Our results offer pharmacological avenues to sensitize therapy-resistant VHL tumours by focusing on the mitochondria.

  • 2.
    Toskas, Konstantinos
    et al.
    Department of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.
    Yaghmaeian-Salmani, Behzad
    Department of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.
    Skiteva, Olga
    Department of Physiology and Pharmacology, Karolinska Institutet, Visionsgatan 4, Solna, Sweden.
    Paslawski, Wojciech
    Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Gillberg, Linda
    Department of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.
    Skara, Vasiliki
    Department of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.
    Antoniou, Irene
    Department of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.
    Södersten, Erik
    Department of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.
    Svenningsson, Per
    Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Chergui, Karima
    Department of Physiology and Pharmacology, Karolinska Institutet, Visionsgatan 4, Solna, Sweden.
    Ringnér, Markus
    Department of Biology, National Bioinformatics Infrastructure Sweden, Science for Life Laboratory, Lund University, Sölvegatan 35, Lund, Sweden.
    Perlmann, Thomas
    Department of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.
    Holmberg, Johan
    Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten). Department of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.
    PRC2-mediated repression is essential to maintain identity and function of differentiated dopaminergic and serotonergic neurons2022Ingår i: Science Advances, E-ISSN 2375-2548, Vol. 8, nr 34, artikel-id eabo1543Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    How neurons can maintain cellular identity over an entire life span remains largely unknown. Here, we show that maintenance of identity in differentiated dopaminergic and serotonergic neurons is critically reliant on the Polycomb repressive complex 2 (PRC2). Deletion of the obligate PRC2 component, Eed, in these neurons resulted in global loss of H3K27me3, followed by a gradual activation of genes harboring both H3K27me3 and H3K9me3 modifications. Notably, H3K9me3 was lost at these PRC2 targets before gene activation. Neuronal survival was not compromised; instead, there was a reduction in subtype-specific gene expression and a progressive impairment of dopaminergic and serotonergic neuronal function, leading to behavioral deficits characteristic of Parkinson's disease and anxiety. Single-cell analysis revealed subtype-specific vulnerability to loss of PRC2 repression in dopamine neurons of the substantia nigra. Our study reveals that a PRC2-dependent nonpermissive chromatin state is essential to maintain the subtype identity and function of dopaminergic and serotonergic neurons.

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