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
Main Authors: 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
Format: Article
Language:English
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
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Summary: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.
ISSN:1662-5102
1662-5102
DOI:10.3389/fncel.2022.869398