Recruitment of Staufen2 Enhances Dendritic Localization of an Intron-Containing CaMKIIα mRNA.
| Autor: | Ortiz R; Molecular Biology Institute of Barcelona (IBMB-CSIC), 08028 Barcelona, Catalonia, Spain., Georgieva MV; Molecular Biology Institute of Barcelona (IBMB-CSIC), 08028 Barcelona, Catalonia, Spain., Gutiérrez S; Molecular Biology Institute of Barcelona (IBMB-CSIC), 08028 Barcelona, Catalonia, Spain., Pedraza N; Institut de Recerca Biomèdica de Lleida (IRBLleida), Departament de Ciències Mèdiques Bàsiques, Universitat de Lleida, 25198 Lleida, Catalonia, Spain., Fernández-Moya SM; Biomedical Center, Division of Anatomy and Cell Biology, Ludwig Maximilians University, 82152 Planegg-Martinsried, Germany., Gallego C; Molecular Biology Institute of Barcelona (IBMB-CSIC), 08028 Barcelona, Catalonia, Spain. Electronic address: cggbmc@ibmb.csic.es. |
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| Jazyk: | angličtina |
| Zdroj: | Cell reports [Cell Rep] 2017 Jul 05; Vol. 20 (1), pp. 13-20. |
| DOI: | 10.1016/j.celrep.2017.06.026 |
| Abstrakt: | 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 mRNA 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 mRNA 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. (Copyright © 2017 The Author(s). Published by Elsevier Inc. All rights reserved.) |
| Databáze: | MEDLINE |
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