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dc.contributor.authorMcFleder, Rhonda L.
dc.contributor.authorMansur, Fernanda
dc.contributor.authorRichter, Joel D.
dc.date2022-08-11T08:08:56.000
dc.date.accessioned2022-08-23T16:12:49Z
dc.date.available2022-08-23T16:12:49Z
dc.date.issued2017-07-18
dc.date.submitted2017-08-29
dc.identifier.citation<p>Cell Rep. 2017 Jul 18;20(3):683-696. doi: 10.1016/j.celrep.2017.06.078. <a href="https://doi.org/10.1016/j.celrep.2017.06.078">Link to article on publisher's website</a></p>
dc.identifier.issn2211-1247
dc.identifier.doi10.1016/j.celrep.2017.06.078
dc.identifier.pmid28723570
dc.identifier.urihttp://hdl.handle.net/20.500.14038/33477
dc.description.abstractTranslation of mRNAs in dendrites mediates synaptic plasticity, the probable cellular basis of learning and memory. Coordination of translational inhibitory and stimulatory mechanisms, as well as dendritic transport of mRNA, is necessary to ensure proper control of this local translation. Here, we find that the deadenylase CNOT7 dynamically regulates dendritic mRNA translation and transport, as well as synaptic plasticity and higher cognitive function. In cultured hippocampal neurons, synaptic stimulation induces a rapid decrease in CNOT7, which, in the short-term, results in poly(A) tail lengthening of target mRNAs. However, at later times following stimulation, decreased poly(A) and dendritic localization of mRNA take place, similar to what is observed when CNOT7 is depleted over several days. In mice, CNOT7 is essential for hippocampal-dependent learning and memory. This study identifies CNOT7 as an important regulator of RNA transport and translation in dendrites, as well as higher cognitive function.
dc.language.isoen_US
dc.relation<p><a href="https://www.ncbi.nlm.nih.gov/pubmed/28723570/">Link to article in PubMed</a></p>
dc.rightsCopyright 2017 The Author(s)
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subjectCNOT7
dc.subjectpolyadenylation
dc.subjectdeadenylation
dc.subjecttranslation
dc.subjectRNA transport
dc.subjectBiochemistry
dc.subjectMolecular and Cellular Neuroscience
dc.titleDynamic Control of Dendritic mRNA Expression by CNOT7 Regulates Synaptic Efficacy and Higher Cognitive Function
dc.typeJournal Article
dc.source.journaltitleCell Reports
dc.source.volume20
dc.source.issue3
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=3025&amp;context=gsbs_sp&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/2003
dc.identifier.contextkey10674660
refterms.dateFOA2022-08-23T16:12:49Z
html.description.abstract<p>Translation of mRNAs in dendrites mediates synaptic plasticity, the probable cellular basis of learning and memory. Coordination of translational inhibitory and stimulatory mechanisms, as well as dendritic transport of mRNA, is necessary to ensure proper control of this local translation. Here, we find that the deadenylase CNOT7 dynamically regulates dendritic mRNA translation and transport, as well as synaptic plasticity and higher cognitive function. In cultured hippocampal neurons, synaptic stimulation induces a rapid decrease in CNOT7, which, in the short-term, results in poly(A) tail lengthening of target mRNAs. However, at later times following stimulation, decreased poly(A) and dendritic localization of mRNA take place, similar to what is observed when CNOT7 is depleted over several days. In mice, CNOT7 is essential for hippocampal-dependent learning and memory. This study identifies CNOT7 as an important regulator of RNA transport and translation in dendrites, as well as higher cognitive function.</p>
dc.identifier.submissionpathgsbs_sp/2003
dc.contributor.departmentProgram in Molecular Medicine
dc.source.pages683-696
dc.contributor.studentRhonda L. McFleder


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