CTCF variants in 39 individuals with a variable neurodevelopmental disorder broaden the mutational and clinical spectrum.

We chose Drosophila as a model because existence of a viable hypomorphic mutant and tissue-specific knockdown and overexpression could circumvent lethality. In contrast to observations of reduced dendritic arborization and spine numbers in mice, 32 , 37 we did not observe alterations in Drosophila larval dendritic arborization neurons or neuromuscular junctions upon knockdown of Ctcf and only mildly significant changes of dendritic length upon overexpression.

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