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Journal Article

The brain-specific double-stranded RNA-binding protein Staufen2 is required for dendritic spine morphogenesis

MPS-Authors
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Goetze,  B
Research Group Molecular Events at the Mammalian Synapse, Max Planck Institute for Developmental Biology, Max Planck Society;

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Tuebing,  F
Research Group Molecular Events at the Mammalian Synapse, Max Planck Institute for Developmental Biology, Max Planck Society;

/persons/resource/persons281241

Xie,  Y
Research Group Molecular Events at the Mammalian Synapse, Max Planck Institute for Developmental Biology, Max Planck Society;

/persons/resource/persons275712

Thomas,  S
Research Group Molecular Events at the Mammalian Synapse, Max Planck Institute for Developmental Biology, Max Planck Society;

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Macchi,  P
Research Group Molecular Events at the Mammalian Synapse, Max Planck Institute for Developmental Biology, Max Planck Society;

/persons/resource/persons275708

Kiebler,  MA
Research Group Molecular Events at the Mammalian Synapse, Max Planck Institute for Developmental Biology, Max Planck Society;

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Citation

Goetze, B., Tuebing, F., Xie, Y., Dorostkar, M., Thomas, S., Pehl, U., et al. (2006). The brain-specific double-stranded RNA-binding protein Staufen2 is required for dendritic spine morphogenesis. The Journal of Cell Biology, 172(2), 221-231. doi:10.1083/jcb.200509035.


Cite as: https://hdl.handle.net/21.11116/0000-000B-30AA-F
Abstract
Mammalian Staufen2 (Stau2) is a member of the double-stranded RNA-binding protein family. Its expression is largely restricted to the brain. It is thought to play a role in the delivery of RNA to dendrites of polarized neurons. To investigate the function of Stau2 in mature neurons, we interfered with Stau2 expression by RNA interference (RNAi). Mature neurons lacking Stau2 displayed a significant reduction in the number of dendritic spines and an increase in filopodia-like structures. The number of PSD95-positive synapses and miniature excitatory postsynaptic currents were markedly reduced in Stau2 down-regulated neurons. Akin effects were caused by overexpression of dominant-negative Stau2. The observed phenotype could be rescued by overexpression of two RNAi cleavage-resistant Stau2 isoforms. In situ hybridization revealed reduced expression levels of beta-actin mRNA and fewer dendritic beta-actin mRNPs in Stau2 down-regulated neurons. Thus, our data suggest an important role for Stau2 in the formation and maintenance of dendritic spines of hippocampal neurons.