Accéder au contenu
Merck

Loss-of-function mutations in UDP-Glucose 6-Dehydrogenase cause recessive developmental epileptic encephalopathy.

Nature communications (2020-02-01)
Holger Hengel, Célia Bosso-Lefèvre, George Grady, Emmanuelle Szenker-Ravi, Hankun Li, Sarah Pierce, Élise Lebigot, Thong-Teck Tan, Michelle Y Eio, Gunaseelan Narayanan, Kagistia Hana Utami, Monica Yau, Nader Handal, Werner Deigendesch, Reinhard Keimer, Hiyam M Marzouqa, Meral Gunay-Aygun, Michael J Muriello, Helene Verhelst, Sarah Weckhuysen, Sonal Mahida, Sakkubai Naidu, Terrence G Thomas, Jiin Ying Lim, Ee Shien Tan, Damien Haye, Michèl A A P Willemsen, Renske Oegema, Wendy G Mitchell, Tyler Mark Pierson, Marisa V Andrews, Marcia C Willing, Lance H Rodan, Tahsin Stefan Barakat, Marjon van Slegtenhorst, Ralitza H Gavrilova, Diego Martinelli, Tal Gilboa, Abdullah M Tamim, Mais O Hashem, Moeenaldeen D AlSayed, Maha M Abdulrahim, Mohammed Al-Owain, Ali Awaji, Adel A H Mahmoud, Eissa A Faqeih, Ali Al Asmari, Sulwan M Algain, Lamyaa A Jad, Hesham M Aldhalaan, Ingo Helbig, David A Koolen, Angelika Riess, Ingeborg Kraegeloh-Mann, Peter Bauer, Suleyman Gulsuner, Hannah Stamberger, Alvin Yu Jin Ng, Sha Tang, Sumanty Tohari, Boris Keren, Laura E Schultz-Rogers, Eric W Klee, Sabina Barresi, Marco Tartaglia, Hagar Mor-Shaked, Sateesh Maddirevula, Amber Begtrup, Aida Telegrafi, Rolph Pfundt, Rebecca Schüle, Brian Ciruna, Carine Bonnard, Mahmoud A Pouladi, James C Stewart, Adam Claridge-Chang, Dirk J Lefeber, Fowzan S Alkuraya, Ajay S Mathuru, Byrappa Venkatesh, Joseph J Barycki, Melanie A Simpson, Saumya S Jamuar, Ludger Schöls, Bruno Reversade
RÉSUMÉ

Developmental epileptic encephalopathies are devastating disorders characterized by intractable epileptic seizures and developmental delay. Here, we report an allelic series of germline recessive mutations in UGDH in 36 cases from 25 families presenting with epileptic encephalopathy with developmental delay and hypotonia. UGDH encodes an oxidoreductase that converts UDP-glucose to UDP-glucuronic acid, a key component of specific proteoglycans and glycolipids. Consistent with being loss-of-function alleles, we show using patients' primary fibroblasts and biochemical assays, that these mutations either impair UGDH stability, oligomerization, or enzymatic activity. In vitro, patient-derived cerebral organoids are smaller with a reduced number of proliferating neuronal progenitors while mutant ugdh zebrafish do not phenocopy the human disease. Our study defines UGDH as a key player for the production of extracellular matrix components that are essential for human brain development. Based on the incidence of variants observed, UGDH mutations are likely to be a frequent cause of recessive epileptic encephalopathy.

MATÉRIAUX
Référence du produit
Marque
Description du produit

Sigma-Aldrich
Anti-UGDH antibody produced in rabbit, Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution