| Literature DB >> 28055140 |
Martina Skopkova1, Friederike Hennig2, Byung-Sik Shin3, Clesson E Turner4, Daniela Stanikova1,5, Katarina Brennerova5, Juraj Stanik1,5,6, Ute Fischer2, Lyndal Henden7,8, Ulrich Müller9, Daniela Steinberger9,10, Esther Leshinsky-Silver11,12,13, Armand Bottani14, Timea Kurdiova1, Jozef Ukropec1, Olga Nyitrayova15, Miriam Kolnikova16, Iwar Klimes1, Guntram Borck17, Melanie Bahlo7,8, Stefan A Haas18, Joo-Ran Kim3, Leda E Lotspeich-Cole3, Daniela Gasperikova1, Thomas E Dever3, Vera M Kalscheuer2.
Abstract
Impairment of translation initiation and its regulation within the integrated stress response (ISR) and related unfolded-protein response has been identified as a cause of several multisystemic syndromes. Here, we link MEHMO syndrome, whose genetic etiology was unknown, to this group of disorders. MEHMO is a rare X-linked syndrome characterized by profound intellectual disability, epilepsy, hypogonadism and hypogenitalism, microcephaly, and obesity. We have identified a C-terminal frameshift mutation (Ile465Serfs) in the EIF2S3 gene in three families with MEHMO syndrome and a novel maternally inherited missense EIF2S3 variant (c.324T>A; p.Ser108Arg) in another male patient with less severe clinical symptoms. The EIF2S3 gene encodes the γ subunit of eukaryotic translation initiation factor 2 (eIF2), crucial for initiation of protein synthesis and regulation of the ISR. Studies in patient fibroblasts confirm increased ISR activation due to the Ile465Serfs mutation and functional assays in yeast demonstrate that the Ile465Serfs mutation impairs eIF2γ function to a greater extent than tested missense mutations, consistent with the more severe clinical phenotype of the Ile465Serfs male mutation carriers. Thus, we propose that more severe EIF2S3 mutations cause the full MEHMO phenotype, while less deleterious mutations cause a milder form of the syndrome with only a subset of the symptoms.Entities:
Keywords: EIF2S3; MEHMO syndrome; XLID; integrated stress response; translation initiation; unfolded-protein response
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Year: 2017 PMID: 28055140 PMCID: PMC6267786 DOI: 10.1002/humu.23170
Source DB: PubMed Journal: Hum Mutat ISSN: 1059-7794 Impact factor: 4.878