Monoallelic de novo variants in DDX17 cause a novel neurodevelopmental disorder
Eleanor G. SeabyiD, Annie GodwiniD, Valentine Clerc, Géraldine Meyer-DilhetiD, Xavier GrandiD, Tia Fletcher, Laloé MonteiroiD, Valério CarelliiD, Flavia PalomboiD, Marco SeriiD, Giulia OlivucciiD, Mina Grippa, Claudia CiaccioiD, Stefano D’ArrigoiD, Maria Rosaria IasconeiD, Marion Bermudez, Jan FischeriD, Nataliya Di DonatoiD, Sophie Gößwein, Marco L. LeungiD, Daniel C. KoboldtiD, Cortlandt MyersiD, Dennis BartholomewiD, Gudny Anna ArnadottiriD, Kāri StefánssoniD, , Sarah EnnisiD
Abstract
IntroductionDDX17 is an RNA helicase shown to be involved in critical processes during the early phases of neuronal differentiation. Globally, we identified 11 patients with neurodevelopmental phenotypes with de novo monoallelic variants in DDX17. All 11 patients had a neurodevelopmental phenotype, whereby intellectual disability, delayed speech and language, and motor delay predominated. Materials and methodsWe performed in utero cortical electroporation in the brain of developing mice, assessing axon complexity and outgrowth of electroporated neurons, comparing wild-type and Ddx17 knockdown. We then undertook ex vivo cortical electroporation on neuronal progenitors to quantitively assess axonal development at a single cell resolution. Homozygous and heterozygous ddx17 crispant knockouts in Xenopus tropicalis were generated for assessment of morphology, performed behavioural assays, and neuronal outgrowth measurements. We further undertook transcriptomic analysis of neuroblastoma SH-SY5Y cells, to identify differentially expressed genes in DDX17-KD cells compared to controls. ResultsKnockdown of Ddx17 in electroporated mouse neurons in vivo showed delayed neuronal migration as well as decreased cortical axon complexity. Mouse primary cortical neurons revealed reduced axon outgrowth upon knockdown of Ddx17 in vitro. The axon outgrowth phenotype was replicated in crispant ddx17 tadpoles, including in a heterozygous model. Crispant tadpoles had clear functional neural defects and showed an impaired neurobehavioral phenotype. Transcriptomic analysis identified a statistically significant number of differentially expressed genes involved in neurodevelopmental processes in DDX17-KD cells compared to control cells. DiscussionWe have identified a new gene, DDX17, representing a rare cause of neurodevelopmental delay. We provide evidence for the role of the gene and mechanistic basis of dysfunctional neurodevelopment in both mammalian and non-mammalian species.
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