Literature DB >> 34234304

High rate of hypomorphic variants as the cause of inherited ataxia and related diseases: study of a cohort of 366 families.

Mehdi Benkirane1, Cecilia Marelli2, Claire Guissart1, Agathe Roubertie3,4, Elizabeth Ollagnon5, Ariane Choumert6, Frédérique Fluchère7, Fabienne Ory Magne8, Yosra Halleb1, Mathilde Renaud9, Lise Larrieu1, David Baux1, Olivier Patat10, Idriss Bousquet5, Jean-Marie Ravel9, Danielle Cuntz-Shadfar3, Catherine Sarret11, Xavier Ayrignac12, Anne Rolland3, Raoul Morales12, Morgane Pointaux1, Cathy Lieutard-Haag1, Brice Laurens13, Caroline Tillikete14, Emilien Bernard14,15, Martial Mallaret16, Clarisse Carra-Dallière12, Christine Tranchant17, Pierre Meyer3,18, Lena Damaj19, Laurent Pasquier19, Cecile Acquaviva20, Annabelle Chaussenot21, Bertrand Isidor22, Karine Nguyen7, William Camu12, Alexandre Eusebio7, Nicolas Carrière23, Audrey Riquet24, Eric Thouvenot25, Victoria Gonzales12, Emilie Carme3, Shahram Attarian7, Sylvie Odent19, Anna Castrioto16, Claire Ewenczyk26, Perrine Charles26, Laurent Kremer7, Samira Sissaoui27, Nadia Bahi-Buisson27, Elsa Kaphan7, Adrian Degardin23, Bérénice Doray28, Sophie Julia10, Ganaëlle Remerand29, Valerie Fraix16, Lydia Abou Haidar3, Leila Lazaro30, Vincent Laugel31, Frederic Villega32, Cyril Charlin6, Solène Frismand9, Marinha Costa Moreira3, Tatiana Witjas7, Christine Francannet11, Ulrike Walther-Louvier3, Mélanie Fradin19, Brigitte Chabrol33, Joel Fluss34, Eric Bieth10, Giovanni Castelnovo25, Sylvain Vergnet13, Isabelle Meunier4,35, Alain Verloes36, Elise Brischoux-Boucher37, Christine Coubes38, David Geneviève38, Nicolas Lebouc39, Jean Phillipe Azulay7, Mathieu Anheim17, Cyril Goizet40, François Rivier3,18, Pierre Labauge12, Patrick Calvas10, Michel Koenig41.   

Abstract

PURPOSE: Diagnosis of inherited ataxia and related diseases represents a real challenge given the tremendous heterogeneity and clinical overlap of the various causes. We evaluated the efficacy of molecular diagnosis of these diseases by sequencing a large cohort of undiagnosed families.
METHODS: We analyzed 366 unrelated consecutive patients with undiagnosed ataxia or related disorders by clinical exome-capture sequencing. In silico analysis was performed with an in-house pipeline that combines variant ranking and copy-number variant (CNV) searches. Variants were interpreted according to American College of Medical Genetics and Genomics/Association for Molecular Pathology (ACMG/AMP) guidelines.
RESULTS: We established the molecular diagnosis in 46% of the cases. We identified 35 mildly affected patients with causative variants in genes that are classically associated with severe presentations. These cases were explained by the occurrence of hypomorphic variants, but also rarely suspected mechanisms such as C-terminal truncations and translation reinitiation.
CONCLUSION: A significant fraction of the clinical heterogeneity and phenotypic overlap is explained by hypomorphic variants that are difficult to identify and not readily predicted. The hypomorphic C-terminal truncation and translation reinitiation mechanisms that we identified may only apply to few genes, as it relies on specific domain organization and alterations. We identified PEX10 and FASTKD2 as candidates for translation reinitiation accounting for mild disease presentation.
© 2021. The Author(s), under exclusive licence to the American College of Medical Genetics and Genomics.

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Year:  2021        PMID: 34234304     DOI: 10.1038/s41436-021-01250-6

Source DB:  PubMed          Journal:  Genet Med        ISSN: 1098-3600            Impact factor:   8.822


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6.  Mini-Exome Coupled to Read-Depth Based Copy Number Variation Analysis in Patients with Inherited Ataxias.

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