| Literature DB >> 26847928 |
Laurent Jullien1,2, Caroline Kannengiesser3, Laetitia Kermasson1,2, Valérie Cormier-Daire4, Thierry Leblanc5, Jean Soulier6, Arturo Londono-Vallejo7, Jean-Pierre de Villartay1,2, Isabelle Callebaut8, Patrick Revy1,2.
Abstract
The DNA helicase RTEL1 participates in telomere maintenance and genome stability. Biallelic mutations in the RTEL1 gene account for the severe telomere biology disorder characteristic of the Hoyeraal-Hreidarsson syndrome (HH). Here, we report a HH patient (P4) carrying two novel compound heterozygous mutations in RTEL1: a premature stop codon (c.949A>T, p.Lys317*) and an intronic deletion leading to an exon skipping and an in-frame deletion of 25 amino-acids (p.Ile398_Lys422). P4's cells exhibit short and dysfunctional telomeres similarly to other RTEL1-deficient patients. 3D structure predictions indicated that the p.Ile398_Lys422 deletion affects a part of the helicase ARCH domain, which lines the pore formed with the core HD and the iron-sulfur cluster domains and is highly specific of sequences from the eukaryotic XPD family members.Entities:
Keywords: ARCH domain; Hoyeraal-Hreidarsson syndrome; RTEL1; Telomere; XPD
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Year: 2016 PMID: 26847928 DOI: 10.1002/humu.22966
Source DB: PubMed Journal: Hum Mutat ISSN: 1059-7794 Impact factor: 4.878