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  1. Article ; Online: Career pathways, part 13.

    Jourdain, Alexis A / Wang, Feilong

    Nature metabolism

    2024  Volume 6, Issue 1, Page(s) 2–5

    MeSH term(s) Career Mobility ; Career Choice
    Language English
    Publishing date 2024-01-17
    Publishing country Germany
    Document type Journal Article
    ISSN 2522-5812
    ISSN (online) 2522-5812
    DOI 10.1038/s42255-023-00954-0
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  2. Article ; Online: Nucleosides are overlooked fuels in central carbon metabolism.

    Strefeler, Abigail / Blanco-Fernandez, Joan / Jourdain, Alexis A

    Trends in endocrinology and metabolism: TEM

    2024  Volume 35, Issue 4, Page(s) 290–299

    Abstract: From our daily nutrition and synthesis within cells, nucleosides enter the bloodstream and circulate throughout the body and tissues. Nucleosides and nucleotides are classically viewed as precursors of nucleic acids, but recently they have emerged as a ... ...

    Abstract From our daily nutrition and synthesis within cells, nucleosides enter the bloodstream and circulate throughout the body and tissues. Nucleosides and nucleotides are classically viewed as precursors of nucleic acids, but recently they have emerged as a novel energy source for central carbon metabolism. Through catabolism by nucleoside phosphorylases, the ribose sugar group is released and can provide substrates for lower steps in glycolysis. In environments with limited glucose, such as at sites of infection or in the tumor microenvironment (TME), cells can use, and may even require, this alternative energy source. Here, we discuss the implications of these new findings in health and disease and speculate on the potential new roles of nucleosides and nucleic acids in energy metabolism.
    MeSH term(s) Humans ; Nucleosides/metabolism ; Carbon/metabolism ; Nucleotides/metabolism ; Nucleic Acids
    Chemical Substances Nucleosides ; Carbon (7440-44-0) ; Nucleotides ; Nucleic Acids
    Language English
    Publishing date 2024-02-29
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1042384-9
    ISSN 1879-3061 ; 1043-2760
    ISSN (online) 1879-3061
    ISSN 1043-2760
    DOI 10.1016/j.tem.2024.01.013
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2999: Show issues Location:
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  3. Article ; Online: Two-Step Tag-Free Isolation of Mitochondria for Improved Protein Discovery and Quantification.

    Blanco-Fernandez, Joan / Jourdain, Alexis A

    Journal of visualized experiments : JoVE

    2023  , Issue 196

    Abstract: Most physiological and disease processes, from central metabolism to immune response to neurodegeneration, involve mitochondria. The mitochondrial proteome is composed of more than 1,000 proteins, and the abundance of each can vary dynamically in ... ...

    Abstract Most physiological and disease processes, from central metabolism to immune response to neurodegeneration, involve mitochondria. The mitochondrial proteome is composed of more than 1,000 proteins, and the abundance of each can vary dynamically in response to external stimuli or during disease progression. Here, we describe a protocol for isolating high-quality mitochondria from primary cells and tissues. The two-step procedure comprises (1) mechanical homogenization and differential centrifugation to isolate crude mitochondria, and (2) tag-free immune capture of mitochondria to isolate pure organelles and eliminate contaminants. Mitochondrial proteins from each purification stage are analyzed by quantitative mass spectrometry, and enrichment yields are calculated, allowing the discovery of novel mitochondrial proteins by subtractive proteomics. Our protocol provides a sensitive and comprehensive approach to studying mitochondrial content in cell lines, primary cells, and tissues.
    MeSH term(s) Mitochondria/metabolism ; Organelles/metabolism ; Mass Spectrometry ; Cell Line ; Mitochondrial Proteins/metabolism ; Proteome/analysis
    Chemical Substances Mitochondrial Proteins ; Proteome
    Language English
    Publishing date 2023-06-02
    Publishing country United States
    Document type Journal Article ; Video-Audio Media ; Research Support, Non-U.S. Gov't
    ZDB-ID 2259946-0
    ISSN 1940-087X ; 1940-087X
    ISSN (online) 1940-087X
    ISSN 1940-087X
    DOI 10.3791/65252
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  4. Article ; Online: Dead-Seq: Discovering Synthetic Lethal Interactions from Dead Cells Genomics.

    Blanco-Fernandez, Joan / Jourdain, Alexis A

    Methods in molecular biology (Clifton, N.J.)

    2023  Volume 2661, Page(s) 329–342

    Abstract: Pooled genetic screens have revolutionized the field of functional genomics, yet perturbations that decrease fitness, such as those leading to synthetic lethality, have remained difficult to quantify at the genomic level. We and colleagues previously ... ...

    Abstract Pooled genetic screens have revolutionized the field of functional genomics, yet perturbations that decrease fitness, such as those leading to synthetic lethality, have remained difficult to quantify at the genomic level. We and colleagues previously developed "death screening," a protocol based on the purification of dead cells in genetic screens, and used it to identify a set of genes necessary for mitochondrial gene expression, translation, and oxidative phosphorylation (OXPHOS), thus offering new possibilities for the diagnosis of mitochondrial disorders. Here, we describe Dead-Seq, a refined protocol for death screening that is compatible with most pooled screening protocols, including genome-wide CRISPR/Cas9 screening. Dead-Seq converts negative-selection screens into positive-selection screens and generates high-quality data directly from dead cells, at limited sequencing costs.
    MeSH term(s) Genomics/methods ; Genome ; Genetic Testing/methods ; CRISPR-Cas Systems
    Language English
    Publishing date 2023-05-11
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-0716-3171-3_19
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  5. Article ; Online: Recovering from the stress of the COVID-19 pandemic.

    Lewis, Samantha C / Jourdain, Alexis A / Schulman, Brenda A / Vousden, Karen H / Fabius, Jacqueline M / Liu, Haipeng

    Molecular cell

    2024  Volume 84, Issue 1, Page(s) 8–11

    Abstract: For our special issue on stress, we asked scientists about recovering from the stress of the pandemic, including some who shared insights with us in mid-2020. They discuss the importance of teamwork, reassessing priorities, and the added stresses of the ... ...

    Abstract For our special issue on stress, we asked scientists about recovering from the stress of the pandemic, including some who shared insights with us in mid-2020. They discuss the importance of teamwork, reassessing priorities, and the added stresses of the cost-of-living crisis, funding cuts, and retaining scientists in academia.
    MeSH term(s) Humans ; COVID-19/epidemiology ; Pandemics
    Language English
    Publishing date 2024-01-05
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1415236-8
    ISSN 1097-4164 ; 1097-2765
    ISSN (online) 1097-4164
    ISSN 1097-2765
    DOI 10.1016/j.molcel.2023.11.013
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5055: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
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  6. Article ; Online: Hypoxia and intra-complex genetic suppressors rescue complex I mutants by a shared mechanism.

    Meisel, Joshua D / Miranda, Maria / Skinner, Owen S / Wiesenthal, Presli P / Wellner, Sandra M / Jourdain, Alexis A / Ruvkun, Gary / Mootha, Vamsi K

    Cell

    2024  Volume 187, Issue 3, Page(s) 659–675.e18

    Abstract: The electron transport chain (ETC) of mitochondria, bacteria, and archaea couples electron flow to proton pumping and is adapted to diverse oxygen environments. Remarkably, in mice, neurological disease due to ETC complex I dysfunction is rescued by ... ...

    Abstract The electron transport chain (ETC) of mitochondria, bacteria, and archaea couples electron flow to proton pumping and is adapted to diverse oxygen environments. Remarkably, in mice, neurological disease due to ETC complex I dysfunction is rescued by hypoxia through unknown mechanisms. Here, we show that hypoxia rescue and hyperoxia sensitivity of complex I deficiency are evolutionarily conserved to C. elegans and are specific to mutants that compromise the electron-conducting matrix arm. We show that hypoxia rescue does not involve the hypoxia-inducible factor pathway or attenuation of reactive oxygen species. To discover the mechanism, we use C. elegans genetic screens to identify suppressor mutations in the complex I accessory subunit NDUFA6/nuo-3 that phenocopy hypoxia rescue. We show that NDUFA6/nuo-3(G60D) or hypoxia directly restores complex I forward activity, with downstream rescue of ETC flux and, in some cases, complex I levels. Additional screens identify residues within the ubiquinone binding pocket as being required for the rescue by NDUFA6/nuo-3(G60D) or hypoxia. This reveals oxygen-sensitive coupling between an accessory subunit and the quinone binding pocket of complex I that can restore forward activity in the same manner as hypoxia.
    MeSH term(s) Animals ; Mice ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans/metabolism ; Electron Transport Complex I/metabolism ; Hypoxia/genetics ; Hypoxia/metabolism ; Mitochondria/genetics ; Mitochondria/metabolism ; Oxygen/metabolism
    Chemical Substances Electron Transport Complex I (EC 7.1.1.2) ; Oxygen (S88TT14065)
    Language English
    Publishing date 2024-01-11
    Publishing country United States
    Document type Journal Article
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2023.12.010
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    Zs.A 1167: Show issues Location:
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    Zs.MG 58: Show issues

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  7. Article ; Online: Distinct mitochondrial defects trigger the integrated stress response depending on the metabolic state of the cell.

    Mick, Eran / Titov, Denis V / Skinner, Owen S / Sharma, Rohit / Jourdain, Alexis A / Mootha, Vamsi K

    eLife

    2020  Volume 9

    Abstract: Mitochondrial dysfunction is associated with activation of the integrated stress response (ISR) but the underlying triggers remain unclear. We systematically combined acute mitochondrial inhibitors with genetic tools for compartment-specific NADH ... ...

    Abstract Mitochondrial dysfunction is associated with activation of the integrated stress response (ISR) but the underlying triggers remain unclear. We systematically combined acute mitochondrial inhibitors with genetic tools for compartment-specific NADH oxidation to trace mechanisms linking different forms of mitochondrial dysfunction to the ISR in proliferating mouse myoblasts and in differentiated myotubes. In myoblasts, we find that impaired NADH oxidation upon electron transport chain (ETC) inhibition depletes asparagine, activating the ISR via the eIF2α kinase GCN2. In myotubes, however, impaired NADH oxidation following ETC inhibition neither depletes asparagine nor activates the ISR, reflecting an altered metabolic state. ATP synthase inhibition in myotubes triggers the ISR via a distinct mechanism related to mitochondrial inner-membrane hyperpolarization. Our work dispels the notion of a universal path linking mitochondrial dysfunction to the ISR, instead revealing multiple paths that depend both on the nature of the mitochondrial defect and on the metabolic state of the cell.
    MeSH term(s) Animals ; Asparagine/metabolism ; Cell Line ; Humans ; Metabolome/genetics ; Metabolome/physiology ; Mice ; Mitochondria/metabolism ; Mitochondria/pathology ; Muscle Fibers, Skeletal/metabolism ; Myoblasts/metabolism ; NAD/metabolism ; Oxidation-Reduction ; Stress, Physiological/genetics ; Stress, Physiological/physiology ; Transcriptome/genetics ; Transcriptome/physiology
    Chemical Substances NAD (0U46U6E8UK) ; Asparagine (7006-34-0)
    Language English
    Publishing date 2020-05-28
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2687154-3
    ISSN 2050-084X ; 2050-084X
    ISSN (online) 2050-084X
    ISSN 2050-084X
    DOI 10.7554/eLife.49178
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  8. Article ; Online: The mitochondrial succinate dehydrogenase complex controls the STAT3-IL-10 pathway in inflammatory macrophages.

    Gobelli, Dino / Serrano-Lorenzo, Pablo / Esteban-Amo, María J / Serna, Julia / Pérez-García, M Teresa / Orduña, Antonio / Jourdain, Alexis A / Martín-Casanueva, Miguel Á / Á de la Fuente, Miguel / Simarro, María

    iScience

    2023  Volume 26, Issue 8, Page(s) 107473

    Abstract: The functions of macrophages are tightly regulated by their metabolic state. However, the role of the mitochondrial electron transport chain (ETC) in macrophage functions remains understudied. Here, we provide evidence that the succinate dehydrogenase ( ... ...

    Abstract The functions of macrophages are tightly regulated by their metabolic state. However, the role of the mitochondrial electron transport chain (ETC) in macrophage functions remains understudied. Here, we provide evidence that the succinate dehydrogenase (SDH)/complex II (CII) is required for respiration and plays a role in controlling effector responses in macrophages. We find that the absence of the catalytic subunits Sdha and Sdhb in macrophages impairs their ability to effectively stabilize HIF-1α and produce the pro-inflammatory cytokine IL-1β in response to LPS stimulation. We also arrive at the novel result that both subunits are essential for the LPS-driven production of IL-10, a potent negative feedback regulator of the macrophage inflammatory response. This phenomenon is explained by the fact that the absence of Sdha and Sdhb leads to the inhibition of Stat3 tyrosine phosphorylation, caused partially by the excessive accumulation of mitochondrial reactive oxygen species (mitoROS) in the knockout cells.
    Language English
    Publishing date 2023-07-25
    Publishing country United States
    Document type Journal Article
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2023.107473
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  9. Article ; Online: Salvage of ribose from uridine or RNA supports glycolysis in nutrient-limited conditions.

    Skinner, Owen S / Blanco-Fernández, Joan / Goodman, Russell P / Kawakami, Akinori / Shen, Hongying / Kemény, Lajos V / Joesch-Cohen, Lena / Rees, Matthew G / Roth, Jennifer A / Fisher, David E / Mootha, Vamsi K / Jourdain, Alexis A

    Nature metabolism

    2023  Volume 5, Issue 5, Page(s) 765–776

    Abstract: Glucose is vital for life, serving as both a source of energy and carbon building block for growth. When glucose is limiting, alternative nutrients must be harnessed. To identify mechanisms by which cells can tolerate complete loss of glucose, we ... ...

    Abstract Glucose is vital for life, serving as both a source of energy and carbon building block for growth. When glucose is limiting, alternative nutrients must be harnessed. To identify mechanisms by which cells can tolerate complete loss of glucose, we performed nutrient-sensitized genome-wide genetic screens and a PRISM growth assay across 482 cancer cell lines. We report that catabolism of uridine from the medium enables the growth of cells in the complete absence of glucose. While previous studies have shown that uridine can be salvaged to support pyrimidine synthesis in the setting of mitochondrial oxidative phosphorylation deficiency
    MeSH term(s) Ribose/metabolism ; Uridine/metabolism ; RNA/metabolism ; Glycolysis ; Humans ; Cell Line, Tumor ; Oxidative Phosphorylation ; Culture Media ; Glucose ; K562 Cells ; Cell Proliferation ; Pentose Phosphate Pathway
    Chemical Substances Ribose (681HV46001) ; Uridine (WHI7HQ7H85) ; RNA (63231-63-0) ; Culture Media ; Glucose (IY9XDZ35W2) ; UPP1 protein, human (EC 2.4.2.3)
    Language English
    Publishing date 2023-05-17
    Publishing country Germany
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2522-5812
    ISSN (online) 2522-5812
    DOI 10.1038/s42255-023-00774-2
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  10. Article ; Online: Mitochondrial RNA granules: Compartmentalizing mitochondrial gene expression.

    Jourdain, Alexis A / Boehm, Erik / Maundrell, Kinsey / Martinou, Jean-Claude

    The Journal of cell biology

    2016  Volume 212, Issue 6, Page(s) 611–614

    Abstract: In mitochondria, DNA replication, gene expression, and RNA degradation machineries coexist within a common nondelimited space, raising the question of how functional compartmentalization of gene expression is achieved. Here, we discuss the recently ... ...

    Abstract In mitochondria, DNA replication, gene expression, and RNA degradation machineries coexist within a common nondelimited space, raising the question of how functional compartmentalization of gene expression is achieved. Here, we discuss the recently characterized "mitochondrial RNA granules," mitochondrial subdomains with an emerging role in the regulation of gene expression.
    MeSH term(s) DNA Replication/genetics ; Gene Expression/genetics ; Genes, Mitochondrial/genetics ; Humans ; Mitochondria/genetics ; RNA/genetics
    Chemical Substances RNA, mitochondrial ; RNA (63231-63-0)
    Language English
    Publishing date 2016-03-14
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218154-x
    ISSN 1540-8140 ; 0021-9525
    ISSN (online) 1540-8140
    ISSN 0021-9525
    DOI 10.1083/jcb.201507125
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