| Literature DB >> 29052317 |
Isabel Hardee1, Ariane Soldatos1, Mariska Davids1, Thierry Vilboux2,3, Camilo Toro1,4, Karen L David5, Carlos R Ferreira4, Michele Nehrebecky1, Joseph Snow6, Audrey Thurm6, Theo Heller7, Ellen F Macnamara1,4, Meral Gunay-Aygun2,4,8, Wadih M Zein9, William A Gahl1,2,4, May Christine V Malicdan1,2,4.
Abstract
Joubert syndrome is a neurodevelopmental disorder, characterized by malformation of the mid and hindbrain leading to the pathognomonic molar tooth appearance of the brainstem and cerebellum on axial MRI. Core clinical manifestations include hypotonia, tachypnea/apnea, ataxia, ocular motor apraxia, and developmental delay of varying degrees. In addition, a subset of patients has retinal dystrophy, chorioretinal colobomas, hepatorenal fibrocystic disease, and polydactyly. Joubert syndrome exhibits genetic heterogeneity, with mutations identified in more than 30 genes, including INPP5E, a gene encoding inositol polyphosphate 5-phosphatase E, which is important in the development and stability of the primary cilium. Here, we report the detailed clinical phenotypes of two sisters with a novel homozygous variant in INPP5E (NM_019892.4: c.1565G>C, NP_063945.2: p.Gly552Ala), expanding the phenotype associated with Joubert syndrome type 1. Expression studies using patient-derived fibroblasts showed changes in mRNA and protein levels. Analysis of fibroblasts from patients revealed that a significant number of cells had shorter or no cilia, indicating defects in ciliogenesis, and cilia maintenance.Entities:
Keywords: INPP5E; Joubert syndrome; ciliopathy; molar-tooth sign; rare disorders
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Year: 2017 PMID: 29052317 PMCID: PMC5685896 DOI: 10.1002/ajmg.a.38376
Source DB: PubMed Journal: Am J Med Genet A ISSN: 1552-4825 Impact factor: 2.802