구.추천논문
Abstract
Jun-Young Oh1, Ara Kwon1, Anna Jo1, Hoon Kim2, Yong-Sook Goo3, Jin-A Lee4 and Hyong Kyu Kim1,*
1Department of Medicine and Microbiology, College of Medicine, Signaling Disorder Research Center, Chungbuk National University, Cheongju, 361-763, The Republic of Korea
2Department of Emergency Medicine, College of Medicine, Chungbuk National University, Cheongju, 361-763, The Republic of Korea
3Department of Physiology, College of Medicine, Chungbuk National University, Cheongju, 361-763, The Republic of Korea
4Department of Biological Engineering, Hannam University, Daejeon, 306-791, The Republic of Korea
*Author for correspondence : Hyong Kyu Kim
Summary
In neurons, transport of a subset of mRNAs to subcellular regions and their translation has a role in synaptic plasticity. Recent studies have suggested a control mechanism of this local translation through mRNA compartmentalization or degradation. Here we report that processing bodies (P-bodies), which are involved in mRNA degradation or storage, are transported to dendrites by conventional kinesin (KIF5A) as a motor protein. Neuronal activation induced by depolarization increased the colocalization of P-bodies with PSD-95 in dendrites. This neuronal activity increased the release of Nd1 and Arp2 mRNA from the P-bodies and, consequently, reversed the decrease of F-actin (induced by overexpression of Dcp1a) in the dendrites. Our data suggest that the activity-induced redistribution of P-bodies and mRNA release from P-bodies might have a role in synaptic structural plasticity by altering levels of mRNAs that are involved in the dynamics of the actin cytoskeleton in dendrites.
Key words : P-bodies, Kinesin motor protein, PSD-95, Actin cytoskeleton, Synaptic plasticity
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