The Kinesin KIF1Bß links neuroblastoma and neurodegenerative disease through anterograde transport of TRKA

We recently identified pathogenic KIF1Bb mutations in sympathetic nervous system malignancies that are defective in developmental apoptosis. Here we deleted KIF1Bb in the mouse sympathetic nervous system based on a cre recombination system driven by the dopamine beta hydroxylase (DBH) promoter. We observed impaired sympathetic nervous function and misexpression of genes required for sympathoadrenal lineage differentiation in KIF1Bb deficient sympathetic ganglia. Overall design: We analyzed superior cervical ganglia from post-natal day 1 mice. We compared ganglia from four wild-type control animals (KIF1Bb fl/fl) with ganglia from four animals with conditional knockout of KIF1Bb (KIF1Bb fl/fl : DBHcre +/-).

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Fell SM, Li S, Wallis K, Kock A, Surova O, Rraklli V, Höfig CS, Li W, Mittag J, Henriksson MA, Kenchappa RS, Holmberg J, Kogner P, Schlisio S