| Literature DB >> 29286390 |
Valerio Conti1, Aurelie Carabalona2, Emilie Pallesi-Pocachard3, Richard J Leventer4, Fabienne Schaller5, Elena Parrini1, Agathe A Deparis6, Françoise Watrin6, Emmanuelle Buhler5, Francesca Novara7, Stefano Lise8, Alistair T Pagnamenta8, Usha Kini9, Jenny C Taylor8, Orsetta Zuffardi10, Alfonso Represa6, David Antony Keays11, Renzo Guerrini12, Antonio Falace6, Carlos Cardoso13.
Abstract
Birth defects that involve the cerebral cortex - also known as malformations of cortical development (MCD) - are important causes of intellectual disability and account for 20-40% of drug-resistant epilepsy in childhood. High-resolution brain imaging has facilitated in vivo identification of a large group of MCD phenotypes. Despite the advances in brain imaging, genomic analysis and generation of animal models, a straightforward workflow to systematically prioritize candidate genes and to test functional effects of putative mutations is missing. To overcome this problem, an experimental strategy enabling the identification of novel causative genes for MCD was developed and validated. This strategy is based on identifying candidate genomic regions or genes via array-CGH or whole-exome sequencing and characterizing the effects of their inactivation or of overexpression of specific mutations in developing rodent brains via in utero electroporation. This approach led to the identification of the C6orf70 gene, encoding for a putative vesicular protein, to the pathogenesis of periventricular nodular heterotopia, a MCD caused by defective neuronal migration.Entities:
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Year: 2017 PMID: 29286390 PMCID: PMC5755514 DOI: 10.3791/53570
Source DB: PubMed Journal: J Vis Exp ISSN: 1940-087X Impact factor: 1.355