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| Home > Publications Database > FOXG1 Regulates PRKAR2B Transcriptionally and Posttranscriptionally via miR200 in the Adult Hippocampus. |
| Home > Publications Database > FOXG1 Regulates PRKAR2B Transcriptionally and Posttranscriptionally via miR200 in the Adult Hippocampus. |
| Journal Article | DZNE-2020-07244 |
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2019
Humana Press
Totowa, NJ
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Please use a persistent id in citations: doi:10.1007/s12035-018-1444-7
Abstract: Rett syndrome is a complex neurodevelopmental disorder that is mainly caused by mutations in MECP2. However, mutations in FOXG1 cause a less frequent form of atypical Rett syndrome, called FOXG1 syndrome. FOXG1 is a key transcription factor crucial for forebrain development, where it maintains the balance between progenitor proliferation and neuronal differentiation. Using genome-wide small RNA sequencing and quantitative proteomics, we identified that FOXG1 affects the biogenesis of miR200b/a/429 and interacts with the ATP-dependent RNA helicase, DDX5/p68. Both FOXG1 and DDX5 associate with the microprocessor complex, whereby DDX5 recruits FOXG1 to DROSHA. RNA-Seq analyses of Foxg1cre/+ hippocampi and N2a cells overexpressing miR200 family members identified cAMP-dependent protein kinase type II-beta regulatory subunit (PRKAR2B) as a target of miR200 in neural cells. PRKAR2B inhibits postsynaptic functions by attenuating protein kinase A (PKA) activity; thus, increased PRKAR2B levels may contribute to neuronal dysfunctions in FOXG1 syndrome. Our data suggest that FOXG1 regulates PRKAR2B expression both on transcriptional and posttranscriptional levels.
Keyword(s): Age Factors (MeSH) ; Animals (MeSH) ; Cyclic AMP-Dependent Protein Kinase RIIbeta Subunit: genetics (MeSH) ; Cyclic AMP-Dependent Protein Kinase RIIbeta Subunit: metabolism (MeSH) ; Forkhead Transcription Factors: genetics (MeSH) ; Forkhead Transcription Factors: metabolism (MeSH) ; Hippocampus: growth & development (MeSH) ; Hippocampus: metabolism (MeSH) ; Mice (MeSH) ; Mice, Inbred C57BL (MeSH) ; Mice, Transgenic (MeSH) ; MicroRNAs: genetics (MeSH) ; MicroRNAs: metabolism (MeSH) ; Nerve Tissue Proteins: genetics (MeSH) ; Nerve Tissue Proteins: metabolism (MeSH) ; Transcription, Genetic: physiology (MeSH) ; Cyclic AMP-Dependent Protein Kinase RIIbeta Subunit ; Forkhead Transcription Factors ; Foxg1 protein, mouse ; MicroRNAs ; Mirn200 microRNA, mouse ; Nerve Tissue Proteins ; PRKAR2B protein, human
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