A loss-of-function analysis reveals that endogenous Rem2 promotes functional glutamatergic synapse formation and restricts dendritic complexity.

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dc.contributor.author Moore, Anna R
dc.contributor.author Ghiretti, Amy E
dc.contributor.author Paradis, Suzanne
dc.date.accessioned 2019-02-05T18:23:27Z
dc.date.available 2019-02-05T18:23:27Z
dc.date.issued 2013
dc.identifier.issn 1932-6203
dc.identifier.other PMC3753333
dc.identifier.uri https://hdl.handle.net/10192/36481
dc.description.abstract Rem2 is a member of the RGK family of small Ras-like GTPases whose expression and function is regulated by neuronal activity in the brain. A number of questions still remain as to the endogenous functions of Rem2 in neurons. RNAi-mediated Rem2 knockdown leads to an increase in dendritic complexity and a decrease in functional excitatory synapses, though a recent report challenged the specificity of Rem2-targeted RNAi reagents. In addition, overexpression in a number of cell types has shown that Rem2 can inhibit voltage-gated calcium channel (VGCC) function, while studies employing RNAi-mediated knockdown of Rem2 have failed to observe a corresponding enhancement of VGCC function. To further investigate these discrepancies and determine the endogenous function of Rem2, we took a comprehensive, loss-of-function approach utilizing two independent, validated Rem2-targeted shRNAs to analyze Rem2 function. We sought to investigate the consequence of endogenous Rem2 knockdown by focusing on the three reported functions of Rem2 in neurons: regulation of synapse formation, dendritic morphology, and voltage-gated calcium channels. We conclude that endogenous Rem2 is a positive regulator of functional, excitatory synapse development and a negative regulator of dendritic complexity. In addition, while we are unable to reach a definitive conclusion as to whether the regulation of VGCCs is an endogenous function of Rem2, our study reports important data regarding RNAi reagents for use in future investigation of this issue.
dc.format.extent 1 file
dc.language English
dc.language.iso eng
dc.relation.isversionof https://dx.doi.org/10.1371/journal.pone.0074751
dc.rights Creative Commons Attribution 4.0 International License
dc.rights.uri http://creativecommons.org/licenses/by/4.0/
dc.subject Medicine
dc.subject Q
dc.subject R
dc.subject Science
dc.subject Research Article
dc.subject Hippocampus
dc.subject Dendrites
dc.subject Synapses
dc.subject Cells
dc.subject Cultured
dc.subject Animals
dc.subject Humans
dc.subject Monomeric GTP-Binding Proteins
dc.subject Glutamic Acid
dc.subject DNA Primers
dc.subject RNA Interference
dc.subject Base Sequence
dc.subject HEK293 Cells
dc.title A loss-of-function analysis reveals that endogenous Rem2 promotes functional glutamatergic synapse formation and restricts dendritic complexity.
dc.type Article
dc.contributor.department Department of Biology
dc.relation.journal PloS One
dc.identifier.pmid 23991227


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