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Recruitment of Staufen2 enhances dendritic localization of an intron-containing CaMKIIα mRNA

Ortiz et al. have found that a subset of the total CaMKIIα mRNA population retains an intron in dendrites. Staufen2 interacts with this intron and enhances the distal dendritic localization of unspliced CaMKIIα mRNA. These findings suggest that intron retention could be a mechanism to modulate dendritic localization of synaptic mRNAs.

Regulation of mRNA localization is a conserved cellular process observed in many types of cells and organisms. Asymmetrical mRNA distribution plays a particularly important role in the nervous system where local translation of localized mRNAs represents a key mechanism in synaptic plasticity. CaMKIIα is a very abundant mRNA detected in neurites, consistent with its crucial role at glutamatergic synapses. Here we report the presence of CaMKIIα mRNA isoforms that contain intron i16 in dendrites, RNA granules and synaptoneurosomes from primary neurons and brain. This subpopulation of unspliced mRNAs preferentially localizes to distal dendrites in a synaptic-activity dependent manner. Staufen2, a well-established marker of RNA transport in dendrites, interacts with intron i16 sequences and enhances its distal dendritic localization, pointing to the existence of intron-mediated mechanisms in the molecular pathways that modulate dendritic transport and localization of synaptic mRNAs.


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