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Pumilio-2 Function in the Mouse Nervous System
Coordinated mRNA translation at the synapse is increasingly recognized as a critical mechanism for neuronal regulation. Pumilio, a translational regulator, is known to be involved in neuronal homeostasis and memory formation in Drosophila. Most recently, the mammalian Pumilio homolog Pumilio-2 (Pum2...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3189250/ https://www.ncbi.nlm.nih.gov/pubmed/22016787 http://dx.doi.org/10.1371/journal.pone.0025932 |
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author | Siemen, Henrike Colas, Damien Heller, H. Craig Brüstle, Oliver Reijo Pera, Renee A. |
author_facet | Siemen, Henrike Colas, Damien Heller, H. Craig Brüstle, Oliver Reijo Pera, Renee A. |
author_sort | Siemen, Henrike |
collection | PubMed |
description | Coordinated mRNA translation at the synapse is increasingly recognized as a critical mechanism for neuronal regulation. Pumilio, a translational regulator, is known to be involved in neuronal homeostasis and memory formation in Drosophila. Most recently, the mammalian Pumilio homolog Pumilio-2 (Pum2) has been found to play a role in the mammalian nervous system, in particular in regulating morphology, arborization and excitability of neuronal dendrites, in vitro. However, the role of Pum2 in vivo remains unclear. Here, we report our investigation of the functional and molecular consequences of Pum2 disruption in vivo using an array of neurophysiology, behavioral and gene expression profiling techniques. We used Pum2-deficient mice to monitor in vivo brain activity using EEG and to study behavior traits, including memory, locomotor activity and nesting capacities. Because of the suspected role of Pum2 in neuronal excitability, we also examined the susceptibility to seizure induction. Finally, we used a quantitative gene expression profiling assay to identify key molecular partners of Pum2. We found that Pum2-deficient mice have abnormal behavioral strategies in spatial and object memory test. Additionally, Pum2 deficiency is associated with increased locomotor activity and decreased body weight. We also observed environmentally-induced impairment in nesting behavior. Most importantly, Pum2-deficient mice showed spontaneous EEG abnormalities and had lower seizure thresholds using a convulsing dosage of pentylenetetrazole. Finally, some genes, including neuronal ion channels, were differentially expressed in the hippocampus of Pum2-deficient mice. These findings demonstrate that Pum2 serves key functions in the adult mammalian central nervous system encompassing neuronal excitability and behavioral response to environmental challenges. |
format | Online Article Text |
id | pubmed-3189250 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-31892502011-10-20 Pumilio-2 Function in the Mouse Nervous System Siemen, Henrike Colas, Damien Heller, H. Craig Brüstle, Oliver Reijo Pera, Renee A. PLoS One Research Article Coordinated mRNA translation at the synapse is increasingly recognized as a critical mechanism for neuronal regulation. Pumilio, a translational regulator, is known to be involved in neuronal homeostasis and memory formation in Drosophila. Most recently, the mammalian Pumilio homolog Pumilio-2 (Pum2) has been found to play a role in the mammalian nervous system, in particular in regulating morphology, arborization and excitability of neuronal dendrites, in vitro. However, the role of Pum2 in vivo remains unclear. Here, we report our investigation of the functional and molecular consequences of Pum2 disruption in vivo using an array of neurophysiology, behavioral and gene expression profiling techniques. We used Pum2-deficient mice to monitor in vivo brain activity using EEG and to study behavior traits, including memory, locomotor activity and nesting capacities. Because of the suspected role of Pum2 in neuronal excitability, we also examined the susceptibility to seizure induction. Finally, we used a quantitative gene expression profiling assay to identify key molecular partners of Pum2. We found that Pum2-deficient mice have abnormal behavioral strategies in spatial and object memory test. Additionally, Pum2 deficiency is associated with increased locomotor activity and decreased body weight. We also observed environmentally-induced impairment in nesting behavior. Most importantly, Pum2-deficient mice showed spontaneous EEG abnormalities and had lower seizure thresholds using a convulsing dosage of pentylenetetrazole. Finally, some genes, including neuronal ion channels, were differentially expressed in the hippocampus of Pum2-deficient mice. These findings demonstrate that Pum2 serves key functions in the adult mammalian central nervous system encompassing neuronal excitability and behavioral response to environmental challenges. Public Library of Science 2011-10-07 /pmc/articles/PMC3189250/ /pubmed/22016787 http://dx.doi.org/10.1371/journal.pone.0025932 Text en Siemen et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Siemen, Henrike Colas, Damien Heller, H. Craig Brüstle, Oliver Reijo Pera, Renee A. Pumilio-2 Function in the Mouse Nervous System |
title |
Pumilio-2 Function in the Mouse Nervous System |
title_full |
Pumilio-2 Function in the Mouse Nervous System |
title_fullStr |
Pumilio-2 Function in the Mouse Nervous System |
title_full_unstemmed |
Pumilio-2 Function in the Mouse Nervous System |
title_short |
Pumilio-2 Function in the Mouse Nervous System |
title_sort | pumilio-2 function in the mouse nervous system |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3189250/ https://www.ncbi.nlm.nih.gov/pubmed/22016787 http://dx.doi.org/10.1371/journal.pone.0025932 |
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