Bi-Allelic MARVELD2 Variant Identified with Exome Sequencing in a Consanguineous Multiplex Ghanaian Family Segregating Non-Syndromic Hearing Loss.

通过外显子组测序在加纳近亲多重家族中鉴定出双等位基因 MARVELD2 变异,该家族表现出非综合征性听力损失

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作者:Twumasi Aboagye Elvis, Adadey Samuel Mawuli, Alves de Souza Rios Leonardo, Esoh Kevin K, Wonkam-Tingang Edmond, Xhakaza Lettilia, De Kock Carmen, Schrauwen Isabelle, Amenga-Etego Lucas, Lang Dirk, Awandare Gordon A, Leal Suzanne M, Mowla Shaheen, Wonkam Ambroise
Genetic studies and phenotypic expansion of hearing loss (HL) for people living in Africa are greatly needed. We evaluated the clinical phenotypes of three affected siblings presenting non-syndromic (NS) HL and five unaffected members of a consanguineous Ghanaian family. Analysis of exome sequence data was performed for all affected and one unaffected family members. In-depth genetic and cellular characterization studies were performed to investigate biological significance of the implicated variant using bioinformatic tools and cell-based experimentation. Audiological examinations showed severe-to-profound, bilateral, symmetrical, and post-lingual onset. The whole-exome sequencing (WES) identified a homozygous frameshift variant: MARVEL domain containing 2 (MARVELD2):c.1058dup;p.(Val354Serfs*5) in all affected siblings. This frameshift variant leads to an early stop codon insertion and predicted to be targeted by nonsense medicated decay (mutant protein predicted to lack conserved C-terminal domain if translated). Cell immunofluorescence and immunocytochemistry studies exposed the functional impact of the mutant protein's expression, stability, localization, protein-protein binding, barrier function, and actin cytoskeleton architecture. The identified variant segregates with NSHL in the index Ghanaian family. The data support this nonsense variant as pathogenic, likely to impact the homeostasis of ions, solutes, and other molecules, compromising membrane barrier and signaling in the inner ear spaces.

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