RT Journal Article SR Electronic T1 Vezatin is required for the retrograde axonal transport of endosomes in Drosophila and zebrafish JF bioRxiv FD Cold Spring Harbor Laboratory SP 2020.02.09.940890 DO 10.1101/2020.02.09.940890 A1 Michael A. Spinner A1 Katherine Pinter A1 Catherine M. Drerup A1 Tory G. Herman YR 2020 UL http://biorxiv.org/content/early/2020/02/10/2020.02.09.940890.abstract AB Active transport of organelles within axons is critical for neuronal health. Retrograde axonal transport, in particular, relays neurotrophic signals received by axon terminals to the nucleus and circulates new material among en passant synapses. The single retrograde motor, cytoplasmic dynein, is linked to diverse cargos by adaptors that promote dynein motility. Here we identify Vezatin as a new, cargo-specific regulator of retrograde axonal transport. Loss-of-function mutations in the Drosophila vezatin-like (vezl) gene prevent signaling endosomes containing activated BMP receptors from initiating transport out of motor neuron terminal boutons. vezl loss also decreases the transport of endosomes and dense core vesicles (DCVs) within axon shafts. While vertebrate Vezatin (Vezt) has not previously been implicated in axonal transport, we show that vezt loss in zebrafish impairs the retrograde movement of late endosomes, causing their accumulation in axon terminals. Our work establishes a new, conserved, cargo-specific role for Vezatin proteins in axonal transport.