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Loss of Protein Arginine Methyltransferase 8 Alters Synapse Composition and Function, Resulting in Behavioral Defects

Title
Loss of Protein Arginine Methyltransferase 8 Alters Synapse Composition and Function, Resulting in Behavioral Defects
Authors
Penney, JaySeo, Jinsoo(Kritskiy, Oleg(Elmsaouri, SaraGao, FanPao, Ping-ChiehSu, Susan C.Tsai, Li-Huei
DGIST Authors
Seo, Jinsoo
Issue Date
2017-09
Citation
JOURNAL OF NEUROSCIENCE, 37(36), 8655-8666
Type
Article
Article Type
Article
Keywords
behaviorexcitatory transmissionmouseplasticityPRMT8synaptic proteins
ISSN
0270-6474
Abstract
Diverse molecular mechanisms regulate synaptic composition and function in the mammalian nervous system. The multifunctional protein arginine methyltransferase 8 (PRMT8) possesses both methyltransferase and phospholipase activities. Here we examine the role of this neuron-specific protein in hippocampal plasticity and cognitive function. PRMT8 protein localizes to synaptic sites, and conditional whole-brain Prmt8 deletion results in altered levels of multiple synaptic proteins in the hippocampus, using both male and female mice. Interestingly, these altered protein levels are due to post-transcriptional mechanisms as the corresponding mRNA levels are unaffected. Strikingly, electrophysiological recordings from hippocampal slices of mice lacking PRMT8 reveal multiple defects in excitatory synaptic function and plasticity. Furthermore, behavioral analyses show that PRMT8 conditional knock-out mice exhibit impaired hippocampal-dependent fear learning. Together, these findings establish PRMT8 as an important component of the molecular machinery required for hippocampal neuronal function. © 2017 the authors.
URI
http://hdl.handle.net/20.500.11750/6170
DOI
10.1523/JNEUROSCI.0591-17.2017
Publisher
SOC NEUROSCIENCE
Related Researcher
  • Author Seo, Jinsoo Laboratory of Aging Brain
  • Research Interests iPSC; Alzheimer's disease; Neurodegeneration; Synapse; Neuroscience
Files:
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Collection:
Department of Brain and Cognitive SciencesLaboratory of Aging Brain1. Journal Articles


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