The function of RNA-binding proteins at the synapse: implications for neurodegeneration
Identifieur interne : 001B89 ( Ncbi/Merge ); précédent : 001B88; suivant : 001B90The function of RNA-binding proteins at the synapse: implications for neurodegeneration
Auteurs : Chantelle F. Sephton ; Gang Yu [États-Unis]Source :
- Cellular and Molecular Life Sciences [ 1420-682X ] ; 2015.
Abstract
The loss of synapses is a central event in neurodegenerative diseases. Synaptic proteins are often associated with disease neuropathology, but their role in synaptic loss is not fully understood. Of the many processes involved in sustaining the integrity of synapses, local protein translation can directly impact synaptic formation, communication, and maintenance. RNA-binding proteins and their association with RNA granules serve to regulate mRNA transportation and translation at synapses and in turn regulate the synapse. Genetic mutations in RNA-binding proteins FUS and TDP-43 have been linked with causing neurodegenerative diseases: amyotrophic lateral sclerosis and frontotemporal dementia. The observation that mutations in FUS and TDP-43 coincide with changes in RNA granules provides evidence that dysfunction of RNA metabolism may underlie the mechanism of synaptic loss in these diseases. However, we do not know how mutations in RNA-binding proteins would affect RNA granule dynamics and local translation, or if these alterations would cause neurodegeneration. Further investigation into this area will lead to important insights into how disruption of RNA metabolism and local translation at synapses can cause neurodegenerative diseases.
Url:
DOI: 10.1007/s00018-015-1943-x
PubMed: 26047658
PubMed Central: 4565867
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">The function of RNA-binding proteins at the synapse: implications for neurodegeneration</title>
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<front><div type="abstract" xml:lang="en"><p>The loss of synapses is a central event in
neurodegenerative diseases. Synaptic proteins are often associated with disease neuropathology, but their role in synaptic loss is not fully understood. Of the many processes involved in sustaining the integrity of synapses, local protein translation can directly impact synaptic formation, communication, and maintenance. RNA-binding proteins and their association with RNA granules serve to regulate mRNA transportation and translation at synapses and in turn regulate the synapse. Genetic mutations in RNA-binding proteins FUS and TDP-43 have been linked with causing neurodegenerative diseases: amyotrophic lateral sclerosis and frontotemporal dementia. The observation that mutations in FUS and TDP-43 coincide with changes in RNA granules provides evidence that dysfunction of RNA metabolism may underlie the mechanism of synaptic loss in these diseases. However, we do not know how mutations in RNA-binding proteins would affect RNA granule dynamics and local translation, or if these alterations would cause neurodegeneration. Further investigation into this area will lead to important insights into how disruption of RNA metabolism and local translation at synapses can cause neurodegenerative diseases.</p>
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<pmc article-type="review-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Cell Mol Life Sci</journal-id>
<journal-id journal-id-type="iso-abbrev">Cell. Mol. Life Sci</journal-id>
<journal-title-group><journal-title>Cellular and Molecular Life Sciences</journal-title>
</journal-title-group>
<issn pub-type="ppub">1420-682X</issn>
<issn pub-type="epub">1420-9071</issn>
<publisher><publisher-name>Springer Basel</publisher-name>
<publisher-loc>Basel</publisher-loc>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">26047658</article-id>
<article-id pub-id-type="pmc">4565867</article-id>
<article-id pub-id-type="publisher-id">1943</article-id>
<article-id pub-id-type="doi">10.1007/s00018-015-1943-x</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Review</subject>
</subj-group>
</article-categories>
<title-group><article-title>The function of RNA-binding proteins at the synapse: implications for neurodegeneration</article-title>
</title-group>
<contrib-group><contrib contrib-type="author" corresp="yes"><name><surname>Sephton</surname>
<given-names>Chantelle F.</given-names>
</name>
<address><email>chantelle.sephton.1@ulaval.ca</email>
</address>
<xref ref-type="aff" rid="Aff1"></xref>
</contrib>
<contrib contrib-type="author"><name><surname>Yu</surname>
<given-names>Gang</given-names>
</name>
<xref ref-type="aff" rid="Aff2"></xref>
</contrib>
<aff id="Aff1"><label></label>
Department of Psychiatry and Neuroscience, Institut Universitaire En Santé Mentale de Québec, Université Laval, Quebec, QC G1J 2G3 Canada</aff>
<aff id="Aff2"><label></label>
Department of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX 75390 USA</aff>
</contrib-group>
<pub-date pub-type="epub"><day>6</day>
<month>6</month>
<year>2015</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>6</day>
<month>6</month>
<year>2015</year>
</pub-date>
<pub-date pub-type="ppub"><year>2015</year>
</pub-date>
<volume>72</volume>
<fpage>3621</fpage>
<lpage>3635</lpage>
<history><date date-type="received"><day>31</day>
<month>1</month>
<year>2015</year>
</date>
<date date-type="rev-recd"><day>18</day>
<month>5</month>
<year>2015</year>
</date>
<date date-type="accepted"><day>28</day>
<month>5</month>
<year>2015</year>
</date>
</history>
<permissions><copyright-statement>© The Author(s) 2015</copyright-statement>
<license license-type="OpenAccess"><license-p><bold>Open Access</bold>
This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.</license-p>
</license>
</permissions>
<abstract id="Abs1"><p>The loss of synapses is a central event in
neurodegenerative diseases. Synaptic proteins are often associated with disease neuropathology, but their role in synaptic loss is not fully understood. Of the many processes involved in sustaining the integrity of synapses, local protein translation can directly impact synaptic formation, communication, and maintenance. RNA-binding proteins and their association with RNA granules serve to regulate mRNA transportation and translation at synapses and in turn regulate the synapse. Genetic mutations in RNA-binding proteins FUS and TDP-43 have been linked with causing neurodegenerative diseases: amyotrophic lateral sclerosis and frontotemporal dementia. The observation that mutations in FUS and TDP-43 coincide with changes in RNA granules provides evidence that dysfunction of RNA metabolism may underlie the mechanism of synaptic loss in these diseases. However, we do not know how mutations in RNA-binding proteins would affect RNA granule dynamics and local translation, or if these alterations would cause neurodegeneration. Further investigation into this area will lead to important insights into how disruption of RNA metabolism and local translation at synapses can cause neurodegenerative diseases.</p>
</abstract>
<kwd-group xml:lang="en"><title>Keywords</title>
<kwd>Amyotrophic lateral sclerosis</kwd>
<kwd>Frontotemporal dementia</kwd>
<kwd>Local translation</kwd>
<kwd>RNA granules</kwd>
<kwd>RNP granules</kwd>
<kwd>Stress granules</kwd>
<kwd>FUS</kwd>
<kwd>TDP-43</kwd>
</kwd-group>
<funding-group><award-group><funding-source><institution-wrap><institution-id institution-id-type="FundRef">http://dx.doi.org/10.13039/100000957</institution-id>
<institution>Alzheimer's Association</institution>
</institution-wrap>
</funding-source>
<award-id>NIRG-14-321584</award-id>
<principal-award-recipient><name><surname>Sephton</surname>
<given-names>Chantelle F.</given-names>
</name>
</principal-award-recipient>
</award-group>
<award-group><funding-source><institution-wrap><institution-id institution-id-type="FundRef">http://dx.doi.org/10.13039/501100000143</institution-id>
<institution>Alzheimer Society</institution>
</institution-wrap>
</funding-source>
<award-id>15-29</award-id>
<principal-award-recipient><name><surname>Sephton</surname>
<given-names>Chantelle F.</given-names>
</name>
</principal-award-recipient>
</award-group>
<award-group><funding-source><institution-wrap><institution-id institution-id-type="FundRef">http://dx.doi.org/10.13039/100000957</institution-id>
<institution>Alzheimer's Association</institution>
</institution-wrap>
</funding-source>
<award-id>IIRG-11-205714</award-id>
<principal-award-recipient><name><surname>Yu</surname>
<given-names>Gang</given-names>
</name>
</principal-award-recipient>
</award-group>
</funding-group>
<custom-meta-group><custom-meta><meta-name>issue-copyright-statement</meta-name>
<meta-value>© Springer Basel 2015</meta-value>
</custom-meta>
</custom-meta-group>
</article-meta>
</front>
</pmc>
<affiliations><list><country><li>États-Unis</li>
</country>
<region><li>Texas</li>
</region>
</list>
<tree><noCountry><name sortKey="Sephton, Chantelle F" sort="Sephton, Chantelle F" uniqKey="Sephton C" first="Chantelle F." last="Sephton">Chantelle F. Sephton</name>
</noCountry>
<country name="États-Unis"><region name="Texas"><name sortKey="Yu, Gang" sort="Yu, Gang" uniqKey="Yu G" first="Gang" last="Yu">Gang Yu</name>
</region>
</country>
</tree>
</affiliations>
</record>
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