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Cytoplasmic Polyadenylation Element-Binding Protein 1 Post-transcriptionally Regulates Fragile X Mental Retardation 1 Expression Through 3' Untranslated Region in Central Nervous System Neurons
Fragile X syndrome (FXS) is an inherited intellectual disability caused by a deficiency in Fragile X mental retardation 1 ( ) gene expression. Recent studies have proposed the importance of cytoplasmic polyadenylation element-binding protein 1 (CPEB1) in FXS pathology; however, the molecular interac...
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| Published in: | Frontiers in cellular neuroscience 2022-04, Vol.16, p.869398-869398 |
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| creator | Oe, Souichi Hayashi, Shinichi Tanaka, Susumu Koike, Taro Hirahara, Yukie Seki-Omura, Ryohei Kakizaki, Rio Sakamoto, Sumika Nakano, Yosuke Noda, Yasuko Yamada, Hisao Kitada, Masaaki |
| description | Fragile X syndrome (FXS) is an inherited intellectual disability caused by a deficiency in Fragile X mental retardation 1 (
) gene expression. Recent studies have proposed the importance of cytoplasmic polyadenylation element-binding protein 1 (CPEB1) in FXS pathology; however, the molecular interaction between
mRNA and CPEB1 has not been fully investigated. Here, we revealed that CPEB1 co-localized and interacted with
mRNA in hippocampal and cerebellar neurons and culture cells. Furthermore, CPEB1 knockdown upregulated
mRNA and protein levels and caused aberrant localization of Fragile X mental retardation protein in neurons. In an FXS cell model, CPEB1 knockdown upregulated the mRNA levels of several mitochondria-related genes and rescued the intracellular heat shock protein family A member 9 distribution. These findings suggest that CPEB1 post-transcriptionally regulated
expression through the 3' untranslated region, and that CPEB1 knockdown might affect mitochondrial function. |
| doi_str_mv | 10.3389/fncel.2022.869398 |
| format | article |
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) gene expression. Recent studies have proposed the importance of cytoplasmic polyadenylation element-binding protein 1 (CPEB1) in FXS pathology; however, the molecular interaction between
mRNA and CPEB1 has not been fully investigated. Here, we revealed that CPEB1 co-localized and interacted with
mRNA in hippocampal and cerebellar neurons and culture cells. Furthermore, CPEB1 knockdown upregulated
mRNA and protein levels and caused aberrant localization of Fragile X mental retardation protein in neurons. In an FXS cell model, CPEB1 knockdown upregulated the mRNA levels of several mitochondria-related genes and rescued the intracellular heat shock protein family A member 9 distribution. These findings suggest that CPEB1 post-transcriptionally regulated
expression through the 3' untranslated region, and that CPEB1 knockdown might affect mitochondrial function.</description><identifier>ISSN: 1662-5102</identifier><identifier>EISSN: 1662-5102</identifier><identifier>DOI: 10.3389/fncel.2022.869398</identifier><identifier>PMID: 35496917</identifier><language>eng</language><publisher>Switzerland: Frontiers Research Foundation</publisher><subject>3' Untranslated regions ; Brain ; Cellular Neuroscience ; Central nervous system ; cytoplasmic polyadenylation-binding protein 1 ; DNA methylation ; FMR1 protein ; fragile X mental retardation 1 ; Fragile X syndrome ; Gene expression ; heat shock protein family A member 9 ; Heat shock proteins ; Hippocampus ; Hybridization ; Intellectual disabilities ; Kinases ; Lasers ; Localization ; Mitochondria ; Nervous system ; Neurons ; Plasmids ; Polyadenylation ; Polyclonal antibodies ; Post-transcription ; post-transcriptional regulation ; Proteins ; Transfer RNA</subject><ispartof>Frontiers in cellular neuroscience, 2022-04, Vol.16, p.869398-869398</ispartof><rights>Copyright © 2022 Oe, Hayashi, Tanaka, Koike, Hirahara, Seki-Omura, Kakizaki, Sakamoto, Nakano, Noda, Yamada and Kitada.</rights><rights>2022. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Copyright © 2022 Oe, Hayashi, Tanaka, Koike, Hirahara, Seki-Omura, Kakizaki, Sakamoto, Nakano, Noda, Yamada and Kitada. 2022 Oe, Hayashi, Tanaka, Koike, Hirahara, Seki-Omura, Kakizaki, Sakamoto, Nakano, Noda, Yamada and Kitada</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4748-8c3004404f3f8755280ee574fd70adad64e64247f38b6b148468f2b0c62ff8a73</citedby><cites>FETCH-LOGICAL-c4748-8c3004404f3f8755280ee574fd70adad64e64247f38b6b148468f2b0c62ff8a73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9051318/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9051318/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35496917$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Oe, Souichi</creatorcontrib><creatorcontrib>Hayashi, Shinichi</creatorcontrib><creatorcontrib>Tanaka, Susumu</creatorcontrib><creatorcontrib>Koike, Taro</creatorcontrib><creatorcontrib>Hirahara, Yukie</creatorcontrib><creatorcontrib>Seki-Omura, Ryohei</creatorcontrib><creatorcontrib>Kakizaki, Rio</creatorcontrib><creatorcontrib>Sakamoto, Sumika</creatorcontrib><creatorcontrib>Nakano, Yosuke</creatorcontrib><creatorcontrib>Noda, Yasuko</creatorcontrib><creatorcontrib>Yamada, Hisao</creatorcontrib><creatorcontrib>Kitada, Masaaki</creatorcontrib><title>Cytoplasmic Polyadenylation Element-Binding Protein 1 Post-transcriptionally Regulates Fragile X Mental Retardation 1 Expression Through 3' Untranslated Region in Central Nervous System Neurons</title><title>Frontiers in cellular neuroscience</title><addtitle>Front Cell Neurosci</addtitle><description>Fragile X syndrome (FXS) is an inherited intellectual disability caused by a deficiency in Fragile X mental retardation 1 (
) gene expression. Recent studies have proposed the importance of cytoplasmic polyadenylation element-binding protein 1 (CPEB1) in FXS pathology; however, the molecular interaction between
mRNA and CPEB1 has not been fully investigated. Here, we revealed that CPEB1 co-localized and interacted with
mRNA in hippocampal and cerebellar neurons and culture cells. Furthermore, CPEB1 knockdown upregulated
mRNA and protein levels and caused aberrant localization of Fragile X mental retardation protein in neurons. In an FXS cell model, CPEB1 knockdown upregulated the mRNA levels of several mitochondria-related genes and rescued the intracellular heat shock protein family A member 9 distribution. These findings suggest that CPEB1 post-transcriptionally regulated
expression through the 3' untranslated region, and that CPEB1 knockdown might affect mitochondrial function.</description><subject>3' Untranslated regions</subject><subject>Brain</subject><subject>Cellular Neuroscience</subject><subject>Central nervous system</subject><subject>cytoplasmic polyadenylation-binding protein 1</subject><subject>DNA methylation</subject><subject>FMR1 protein</subject><subject>fragile X mental retardation 1</subject><subject>Fragile X syndrome</subject><subject>Gene expression</subject><subject>heat shock protein family A member 9</subject><subject>Heat shock proteins</subject><subject>Hippocampus</subject><subject>Hybridization</subject><subject>Intellectual disabilities</subject><subject>Kinases</subject><subject>Lasers</subject><subject>Localization</subject><subject>Mitochondria</subject><subject>Nervous system</subject><subject>Neurons</subject><subject>Plasmids</subject><subject>Polyadenylation</subject><subject>Polyclonal antibodies</subject><subject>Post-transcription</subject><subject>post-transcriptional regulation</subject><subject>Proteins</subject><subject>Transfer RNA</subject><issn>1662-5102</issn><issn>1662-5102</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNpdks9u1DAQxiMEoqXwAFyQJQ5wyeJ_cZwLEqy2UKlABa3EzXKSSdaV117spCKPx5vhbErVcrJn5pufPfaXZS8JXjEmq3eda8CuKKZ0JUXFKvkoOyZC0LwgmD6-tz_KnsV4jbGggsun2REreCUqUh5nf9bT4PdWx51p0IW3k27BTVYPxju0sbADN-QfjWuN69FF8AMYh0hSxiEfgnaxCWY_i7W1E_oO_Zh6IaLToHtjAf1EXxJB21QadGgXLkGb3_sAMc7B5Tb4sd8i9gZduQNyJrQzay6n49Yw5y36CuHGjxH9mOIAuxSOwbv4PHvSaRvhxe16kl2dbi7Xn_Pzb5_O1h_O84aXXOayYRhzjnnHOlkWBZUYoCh515ZYt7oVHASnvOyYrEVNuORCdrTGjaBdJ3XJTrKzhdt6fa32wex0mJTXRh0SPvRKh8E0FlRTF1pITmuqO65pWUnQAKyVpMKtKHRivV9Y-7HeQdssAz6APqw4s1W9v1EVLggjMgHe3gKC_zVCHNTOxGQGqx2kJ1JUFFIUnNMqSV__J732Y0j_dVBhRrioZiBZVE3wMQbo7i5DsJrNpg5mU7PZ1GK21PPq_hR3Hf_cxf4CGSLVlQ</recordid><startdate>20220415</startdate><enddate>20220415</enddate><creator>Oe, Souichi</creator><creator>Hayashi, Shinichi</creator><creator>Tanaka, Susumu</creator><creator>Koike, Taro</creator><creator>Hirahara, Yukie</creator><creator>Seki-Omura, Ryohei</creator><creator>Kakizaki, Rio</creator><creator>Sakamoto, Sumika</creator><creator>Nakano, Yosuke</creator><creator>Noda, Yasuko</creator><creator>Yamada, Hisao</creator><creator>Kitada, Masaaki</creator><general>Frontiers Research Foundation</general><general>Frontiers Media S.A</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7XB</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20220415</creationdate><title>Cytoplasmic Polyadenylation Element-Binding Protein 1 Post-transcriptionally Regulates Fragile X Mental Retardation 1 Expression Through 3' Untranslated Region in Central Nervous System Neurons</title><author>Oe, Souichi ; Hayashi, Shinichi ; Tanaka, Susumu ; Koike, Taro ; Hirahara, Yukie ; Seki-Omura, Ryohei ; Kakizaki, Rio ; Sakamoto, Sumika ; Nakano, Yosuke ; Noda, Yasuko ; Yamada, Hisao ; Kitada, Masaaki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4748-8c3004404f3f8755280ee574fd70adad64e64247f38b6b148468f2b0c62ff8a73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>3' Untranslated regions</topic><topic>Brain</topic><topic>Cellular Neuroscience</topic><topic>Central nervous system</topic><topic>cytoplasmic polyadenylation-binding protein 1</topic><topic>DNA methylation</topic><topic>FMR1 protein</topic><topic>fragile X mental retardation 1</topic><topic>Fragile X syndrome</topic><topic>Gene expression</topic><topic>heat shock protein family A member 9</topic><topic>Heat shock proteins</topic><topic>Hippocampus</topic><topic>Hybridization</topic><topic>Intellectual disabilities</topic><topic>Kinases</topic><topic>Lasers</topic><topic>Localization</topic><topic>Mitochondria</topic><topic>Nervous system</topic><topic>Neurons</topic><topic>Plasmids</topic><topic>Polyadenylation</topic><topic>Polyclonal antibodies</topic><topic>Post-transcription</topic><topic>post-transcriptional regulation</topic><topic>Proteins</topic><topic>Transfer RNA</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Oe, Souichi</creatorcontrib><creatorcontrib>Hayashi, Shinichi</creatorcontrib><creatorcontrib>Tanaka, Susumu</creatorcontrib><creatorcontrib>Koike, Taro</creatorcontrib><creatorcontrib>Hirahara, Yukie</creatorcontrib><creatorcontrib>Seki-Omura, Ryohei</creatorcontrib><creatorcontrib>Kakizaki, Rio</creatorcontrib><creatorcontrib>Sakamoto, Sumika</creatorcontrib><creatorcontrib>Nakano, Yosuke</creatorcontrib><creatorcontrib>Noda, Yasuko</creatorcontrib><creatorcontrib>Yamada, Hisao</creatorcontrib><creatorcontrib>Kitada, Masaaki</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest Biological Science Collection</collection><collection>ProQuest Science Journals</collection><collection>ProQuest Biological Science Journals</collection><collection>Publicly Available Content Database (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Frontiers in cellular neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Oe, Souichi</au><au>Hayashi, Shinichi</au><au>Tanaka, Susumu</au><au>Koike, Taro</au><au>Hirahara, Yukie</au><au>Seki-Omura, Ryohei</au><au>Kakizaki, Rio</au><au>Sakamoto, Sumika</au><au>Nakano, Yosuke</au><au>Noda, Yasuko</au><au>Yamada, Hisao</au><au>Kitada, Masaaki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cytoplasmic Polyadenylation Element-Binding Protein 1 Post-transcriptionally Regulates Fragile X Mental Retardation 1 Expression Through 3' Untranslated Region in Central Nervous System Neurons</atitle><jtitle>Frontiers in cellular neuroscience</jtitle><addtitle>Front Cell Neurosci</addtitle><date>2022-04-15</date><risdate>2022</risdate><volume>16</volume><spage>869398</spage><epage>869398</epage><pages>869398-869398</pages><issn>1662-5102</issn><eissn>1662-5102</eissn><abstract>Fragile X syndrome (FXS) is an inherited intellectual disability caused by a deficiency in Fragile X mental retardation 1 (
) gene expression. Recent studies have proposed the importance of cytoplasmic polyadenylation element-binding protein 1 (CPEB1) in FXS pathology; however, the molecular interaction between
mRNA and CPEB1 has not been fully investigated. Here, we revealed that CPEB1 co-localized and interacted with
mRNA in hippocampal and cerebellar neurons and culture cells. Furthermore, CPEB1 knockdown upregulated
mRNA and protein levels and caused aberrant localization of Fragile X mental retardation protein in neurons. In an FXS cell model, CPEB1 knockdown upregulated the mRNA levels of several mitochondria-related genes and rescued the intracellular heat shock protein family A member 9 distribution. These findings suggest that CPEB1 post-transcriptionally regulated
expression through the 3' untranslated region, and that CPEB1 knockdown might affect mitochondrial function.</abstract><cop>Switzerland</cop><pub>Frontiers Research Foundation</pub><pmid>35496917</pmid><doi>10.3389/fncel.2022.869398</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 3' Untranslated regions Brain Cellular Neuroscience Central nervous system cytoplasmic polyadenylation-binding protein 1 DNA methylation FMR1 protein fragile X mental retardation 1 Fragile X syndrome Gene expression heat shock protein family A member 9 Heat shock proteins Hippocampus Hybridization Intellectual disabilities Kinases Lasers Localization Mitochondria Nervous system Neurons Plasmids Polyadenylation Polyclonal antibodies Post-transcription post-transcriptional regulation Proteins Transfer RNA |
| title | Cytoplasmic Polyadenylation Element-Binding Protein 1 Post-transcriptionally Regulates Fragile X Mental Retardation 1 Expression Through 3' Untranslated Region in Central Nervous System Neurons |
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