Cytoplasmic Polyadenylation Element-Binding Protein 1 Post-transcriptionally Regulates Fragile X Mental Retardation 1 Expression Through 3′ Untranslated Region in Central Nervous System Neurons

Bibliographic Details
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
Authors: Souichi Oe, Shinichi Hayashi, Susumu Tanaka, Taro Koike, Yukie Hirahara, Ryohei Seki-Omura, Rio Kakizaki, Sumika Sakamoto, Yosuke Nakano, Yasuko Noda, Hisao Yamada, Masaaki Kitada
Source: Frontiers in Cellular Neuroscience, Vol 16 (2022)
Publisher Information: Frontiers Media S.A., 2022.
Publication Year: 2022
Collection: LCC:Neurosciences. Biological psychiatry. Neuropsychiatry
Subject Terms: cytoplasmic polyadenylation-binding protein 1, fragile X mental retardation 1, heat shock protein family A member 9, mitochondria, post-transcriptional regulation, Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571
More Details: Fragile X syndrome (FXS) is an inherited intellectual disability caused by a deficiency in Fragile X mental retardation 1 (Fmr1) gene expression. Recent studies have proposed the importance of cytoplasmic polyadenylation element-binding protein 1 (CPEB1) in FXS pathology; however, the molecular interaction between Fmr1 mRNA and CPEB1 has not been fully investigated. Here, we revealed that CPEB1 co-localized and interacted with Fmr1 mRNA in hippocampal and cerebellar neurons and culture cells. Furthermore, CPEB1 knockdown upregulated Fmr1 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 Fmr1 expression through the 3′ untranslated region, and that CPEB1 knockdown might affect mitochondrial function.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 1662-5102
Relation: https://www.frontiersin.org/articles/10.3389/fncel.2022.869398/full; https://doaj.org/toc/1662-5102
DOI: 10.3389/fncel.2022.869398
Access URL: https://doaj.org/article/cb5a6842b2af4a2798eaee3d8190d65a
Accession Number: edsdoj.b5a6842b2af4a2798eaee3d8190d65a
Database: Directory of Open Access Journals
More Details
ISSN:16625102
DOI:10.3389/fncel.2022.869398
Published in:Frontiers in Cellular Neuroscience
Language:English