In this work we show that SMN interacts with the RNA binding protein (RBP) HuD in motoneurons in vivo during formation of axonal branches and dendrites. We show this biochemically by performing motoneuron specific biochemistry and by generating novel HuD mutant zebrafish. HuD binds RNAs that are critical for neuronal development particularly of axons and dendrites. We show that disrupting SMN or HuD results in decreased levels of Gap43, an RNA involved in axonal growth. Together these data support that the interaction of SMN with neuronal RBPs is critical for motoneuron development and disruption can contribute to phenotypes observed in spinal muscular atrophy.
In this paper we use genetics, biochemistry, imaging, motor behavior, and RNA analysis.
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