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Subject collection: C. elegans

  • RESEARCH ARTICLE
    Interpreting the pathogenicity of Joubert syndrome missense variants in Caenorhabditis elegans
    Karen I. Lange, Sofia Tsiropoulou, Katarzyna Kucharska, Oliver E. Blacque
    Disease Models & Mechanisms 2021 14: dmm046631 doi: 10.1242/dmm.046631 Published 26 January 2021

    Editor’s choice: Genome editing was carried out in C. elegans to model and characterise two pathogenic missense variants of mksr-2/B9D2, P74S and G155S, from a compound heterozygous patient with Joubert syndrome.

  • RESEARCH ARTICLE
    Modulating the endoplasmic reticulum stress response attenuates neurodegeneration in a Caenorhabditis elegans model of spinal muscular atrophy
    James J. Doyle, Celine Vrancx, Claudia Maios, Audrey Labarre, Shunmoogum A. Patten, J. Alex Parker
    Disease Models & Mechanisms 2020 13: dmm041350 doi: 10.1242/dmm.041350 Published 22 December 2020

    Summary: A new non-larval-lethal C. elegans model of spinal muscular atrophy shows mild phenotypes, such as muscle cell and neuronal degeneration, and is therefore useful for testing potential drug treatments.

  • AT A GLANCE
    Modeling neurodegeneration in Caenorhabditis elegans
    Kim A. Caldwell, Corey W. Willicott, Guy A. Caldwell
    Disease Models & Mechanisms 2020 13: dmm046110 doi: 10.1242/dmm.046110 Published 26 October 2020

    Summary: While unsurpassed as an experimental system for fundamental biology, Caenorhabditis elegans remains undervalued for its translational potential. Here, we highlight significant outcomes from, and resources available for, C. elegans-based research into neurodegenerative disorders.

  • RESEARCH ARTICLE
    The SDHB Arg230His mutation causing familial paraganglioma alters glycolysis in a new Caenorhabditis elegans model
    Éva Saskői, Zoltán Hujber, Gábor Nyírő, István Likó, Barbara Mátyási, Gábor Petővári, Katalin Mészáros, Attila L. Kovács, László Patthy, Shreyas Supekar, Hao Fan, Gergely Sváb, László Tretter, Arunabh Sarkar, Aamir Nazir, Anna Sebestyén, Attila Patócs, Anil Mehta, Krisztina Takács-Vellai
    Disease Models & Mechanisms 2020 13: dmm044925 doi: 10.1242/dmm.044925 Published 15 October 2020

    Editor’s choice: Heritable pheochromocytoma/paraganglioma follows the Arg230His missense mutation in SDHB in mitochondrial complex II. By mutating this highly conserved ortholog in C. elegans, we generated a tractable phenotype.

  • RESEARCH ARTICLE
    Repurposing the aldose reductase inhibitor and diabetic neuropathy drug epalrestat for the congenital disorder of glycosylation PMM2-CDG
    Sangeetha Iyer, Feba S. Sam, Nina DiPrimio, Graeme Preston, Jan Verheijen, Kausalya Murthy, Zachary Parton, Hillary Tsang, Jessica Lao, Eva Morava, Ethan O. Perlstein
    Disease Models & Mechanisms 2019 12: dmm040584 doi: 10.1242/dmm.040584 Published 11 November 2019

    Editor's choice: Drug repurposing screens using worm and patient fibroblast models of PMM2-CDG led to the discovery of epalrestat, the first activator of PMM2 that targets the root cause of disease.

  • RESEARCH ARTICLE
    Drug screens of NGLY1 deficiency in worm and fly models reveal catecholamine, NRF2 and anti-inflammatory-pathway activation as potential clinical approaches
    Sangeetha Iyer, Joshua D. Mast, Hillary Tsang, Tamy P. Rodriguez, Nina DiPrimio, Madeleine Prangley, Feba S. Sam, Zachary Parton, Ethan O. Perlstein
    Disease Models & Mechanisms 2019 12: dmm040576 doi: 10.1242/dmm.040576 Published 4 November 2019

    Summary: Using worm and fly models of an ultra-rare congenital disorder of glycosylation, we performed repurposing screens and identified the FDA-approved drug aripiprazole as a clinical candidate.

  • RESEARCH ARTICLE
    ApoE-associated modulation of neuroprotection from Aβ-mediated neurodegeneration in transgenic Caenorhabditis elegans
    Edward F. Griffin, Samuel E. Scopel, Cayman A. Stephen, Adam C. Holzhauer, Madeline A. Vaji, Ryan A. Tuckey, Laura A. Berkowitz, Kim A. Caldwell, Guy A. Caldwell
    Disease Models & Mechanisms 2019 12: dmm037218 doi: 10.1242/dmm.037218 Published 15 February 2019

    Summary: We report new humanized nematode models of amyloid-beta and apolipoprotein E gene expression, examining readouts for neurodegeneration, behavior, cellular function and survival, to elucidate the relative contributions of the proteins to the underlying pathology of Alzheimer's disease.

  • RESEARCH ARTICLE
    Muscle strength deficiency and mitochondrial dysfunction in a muscular dystrophy model of Caenorhabditis elegans and its functional response to drugs
    Jennifer E. Hewitt, Amelia K. Pollard, Leila Lesanpezeshki, Colleen S. Deane, Christopher J. Gaffney, Timothy Etheridge, Nathaniel J. Szewczyk, Siva A. Vanapalli
    Disease Models & Mechanisms 2018 11: dmm036137 doi: 10.1242/dmm.036137 Published 4 December 2018

    Editor's choice: Dystrophin-deficient Caenorhabditis elegans have measurably weak muscle strength and mitochondrial dysfunction, and they respond to drug treatments standard in treating human Duchenne muscular dystrophy.

  • RESOURCE ARTICLE
    CRISPR-Cas9 human gene replacement and phenomic characterization in Caenorhabditis elegans to understand the functional conservation of human genes and decipher variants of uncertain significance
    Troy A. McDiarmid, Vinci Au, Aaron D. Loewen, Joseph Liang, Kota Mizumoto, Donald G. Moerman, Catharine H. Rankin
    Disease Models & Mechanisms 2018 11: dmm036517 doi: 10.1242/dmm.036517 Published 26 November 2018

    Summary: Here, we provide a CRISPR-Cas9 human gene replacement and phenomic characterization strategy to directly replace Caenorhabditis elegans genes with their human orthologs for disease variant modeling and therapeutic screening.

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