The splicing regulator Rbfox1 (A2BP1) controls neuronal excitation in the mammalian brain
The Rbfox family of RNA binding proteins mediate alternative splicing. Douglas Black and colleagues show that targeted deletion of the mouse Rbfox1 gene in the CNS alters splice isoforms of a subset of genes and is associated with neural hyperexcitability with spontaneous and drug-induced seizures....
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| Published in | Nature genetics Vol. 43; no. 7; pp. 706 - 711 |
|---|---|
| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
New York
Nature Publishing Group US
01.07.2011
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1061-4036 1546-1718 1546-1718 |
| DOI | 10.1038/ng.841 |
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| Abstract | The Rbfox family of RNA binding proteins mediate alternative splicing. Douglas Black and colleagues show that targeted deletion of the mouse
Rbfox1
gene in the CNS alters splice isoforms of a subset of genes and is associated with neural hyperexcitability with spontaneous and drug-induced seizures.
The Rbfox family of RNA binding proteins regulates alternative splicing of many important neuronal transcripts, but its role in neuronal physiology is not clear
1
. We show here that central nervous system–specific deletion of the gene encoding Rbfox1 results in heightened susceptibility to spontaneous and kainic acid–induced seizures. Electrophysiological recording revealed a corresponding increase in neuronal excitability in the dentate gyrus of the knockout mice. Whole-transcriptome analyses identified multiple splicing changes in the
Rbfox1
−/−
brain with few changes in overall transcript abundance. These splicing changes alter proteins that mediate synaptic transmission and membrane excitation. Thus, Rbfox1 directs a genetic program required in the prevention of neuronal hyperexcitation and seizures. The Rbfox1 knockout mice provide a new model to study the post-transcriptional regulation of synaptic function. |
|---|---|
| AbstractList | The Rbfox family of RNA binding proteins regulates alternative splicing of many important neuronal transcripts, but its role in neuronal physiology is not clear1. We show here that central nervous system-specific deletion of the gene encoding Rbfox1 results in heightened susceptibility to spontaneous and kainic acid-induced seizures. Electrophysiological recording revealed a corresponding increase in neuronal excitability in the dentate gyrus of the knockout mice. Whole-transcriptome analyses identified multiple splicing changes in the [Rbfox1.sup.-/-] brain with few changes in overall transcript abundance. These splicing changes alter proteins that mediate synaptic transmission and membrane excitation. Thus, Rbfox1 directs a genetic program required in the prevention of neuronal hyperexcitation and seizures. The Rbfox1 knockout mice provide a new model to study the post-transcriptional regulation of synaptic function. The Rbfox family of RNA binding proteins regulates alternative splicing of many important neuronal transcripts, but its role in neuronal physiology is not clear. We show here that central nervous system-specific deletion of the gene encoding Rbfox1 results in heightened susceptibility to spontaneous and kainic acid-induced seizures. Electrophysiological recording revealed a corresponding increase in neuronal excitability in the dentate gyrus of the knockout mice. Whole-transcriptome analyses identified multiple splicing changes in the Rbfox1(-/-) brain with few changes in overall transcript abundance. These splicing changes alter proteins that mediate synaptic transmission and membrane excitation. Thus, Rbfox1 directs a genetic program required in the prevention of neuronal hyperexcitation and seizures. The Rbfox1 knockout mice provide a new model to study the post-transcriptional regulation of synaptic function.The Rbfox family of RNA binding proteins regulates alternative splicing of many important neuronal transcripts, but its role in neuronal physiology is not clear. We show here that central nervous system-specific deletion of the gene encoding Rbfox1 results in heightened susceptibility to spontaneous and kainic acid-induced seizures. Electrophysiological recording revealed a corresponding increase in neuronal excitability in the dentate gyrus of the knockout mice. Whole-transcriptome analyses identified multiple splicing changes in the Rbfox1(-/-) brain with few changes in overall transcript abundance. These splicing changes alter proteins that mediate synaptic transmission and membrane excitation. Thus, Rbfox1 directs a genetic program required in the prevention of neuronal hyperexcitation and seizures. The Rbfox1 knockout mice provide a new model to study the post-transcriptional regulation of synaptic function. The Rbfox family of RNA binding proteins regulates alternative splicing of many important neuronal transcripts, but its role in neuronal physiology is not clear. We show here that central nervous system-specific deletion of the gene encoding Rbfox1 results in heightened susceptibility to spontaneous and kainic acid-induced seizures. Electrophysiological recording revealed a corresponding increase in neuronal excitability in the dentate gyrus of the knockout mice. Whole-transcriptome analyses identified multiple splicing changes in the Rbfox1(-/-) brain with few changes in overall transcript abundance. These splicing changes alter proteins that mediate synaptic transmission and membrane excitation. Thus, Rbfox1 directs a genetic program required in the prevention of neuronal hyperexcitation and seizures. The Rbfox1 knockout mice provide a new model to study the post-transcriptional regulation of synaptic function. The Rbfox family of RNA binding proteins regulates alternative splicing of many important neuronal transcripts, but its role in neuronal physiology is not clear. We show here that central nervous system-specific deletion of the gene encoding Rbfox1 results in heightened susceptibility to spontaneous and kainic acid-induced seizures. Electrophysiological recording revealed a corresponding increase in neuronal excitability in the dentate gyrus of the knockout mice. Whole-transcriptome analyses identified multiple splicing changes in the Rbfox1 super(-/-) brain with few changes in overall transcript abundance. These splicing changes alter proteins that mediate synaptic transmission and membrane excitation. Thus, Rbfox1 directs a genetic program required in the prevention of neuronal hyperexcitation and seizures. The Rbfox1 knockout mice provide a new model to study the post-transcriptional regulation of synaptic function. The Rbfox family of RNA binding proteins regulates alternative splicing of many important neuronal transcripts but their role in neuronal physiology is not clear 1 . We show here that central nervous system (CNS)-specific deletion of the Rbfox1 gene results in heightened susceptibility to spontaneous and kainic acid-induced seizures. Electrophysiological recording reveals a corresponding increase in neuronal excitability in the dentate gyrus of the knockout mice. Whole transcriptome analyses identify multiple splicing changes in the Rbfox1 −/− brain with few changes in overall transcript abundance. These splicing changes alter proteins that mediate synaptic transmission and membrane excitation, some of which are implicated in human epilepsy. Thus, Rbfox1 directs a genetic program required in the prevention of neuronal hyperexcitation and seizures. The Rbfox1 knockout mice provide a new model to study the post-transcriptional regulation of synaptic function. The Rbfox family of RNA binding proteins regulates alternative splicing of many important neuronal transcripts, but its role in neuronal physiology is not clear. We show here that central nervous system-specific deletion of the gene encoding Rbfox1 results in heightened susceptibility to spontaneous and kainic acid-induced seizures. Electrophysiological recording revealed a corresponding increase in neuronal excitability in the dentate gyrus of the knockout mice. Whole-transcriptome analyses identified multiple splicing changes in the Rbfox1^sup -/-^ brain with few changes in overall transcript abundance. These splicing changes alter proteins that mediate synaptic transmission and membrane excitation. Thus, Rbfox1 directs a genetic program required in the prevention of neuronal hyperexcitation and seizures. The Rbfox1 knockout mice provide a new model to study the post-transcriptional regulation of synaptic function. [PUBLICATION ABSTRACT] The Rbfox family of RNA binding proteins mediate alternative splicing. Douglas Black and colleagues show that targeted deletion of the mouse Rbfox1 gene in the CNS alters splice isoforms of a subset of genes and is associated with neural hyperexcitability with spontaneous and drug-induced seizures. The Rbfox family of RNA binding proteins regulates alternative splicing of many important neuronal transcripts, but its role in neuronal physiology is not clear 1 . We show here that central nervous system–specific deletion of the gene encoding Rbfox1 results in heightened susceptibility to spontaneous and kainic acid–induced seizures. Electrophysiological recording revealed a corresponding increase in neuronal excitability in the dentate gyrus of the knockout mice. Whole-transcriptome analyses identified multiple splicing changes in the Rbfox1 −/− brain with few changes in overall transcript abundance. These splicing changes alter proteins that mediate synaptic transmission and membrane excitation. Thus, Rbfox1 directs a genetic program required in the prevention of neuronal hyperexcitation and seizures. The Rbfox1 knockout mice provide a new model to study the post-transcriptional regulation of synaptic function. |
| Audience | Academic |
| Author | Ares, Manuel Stoilov, Peter Maguire, Jamie Black, Douglas L Damianov, Andrey Shiue, Lily Mody, Istvan Lin, Chia-Ho Gehman, Lauren T |
| AuthorAffiliation | 1 Molecular Biology Institute, University of California, Los Angeles, Los Angeles, California 90095 2 Department of Biochemistry, School of Medicine, West Virginia University, Morgantown, West Virginia 26506 6 Departments of Neurology and Physiology, The David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California 90095 5 Department of Molecular, Cell and Developmental Biology, Sinsheimer Labs, University of California, Santa Cruz, Santa Cruz, California 95064 3 Department of Neuroscience, Tufts University School of Medicine, Boston, Massachusetts 02111 4 Department of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, Los Angeles, California 90095 7 Howard Hughes Medical Institute, University of California, Los Angeles, Los Angeles, California 90095 |
| AuthorAffiliation_xml | – name: 5 Department of Molecular, Cell and Developmental Biology, Sinsheimer Labs, University of California, Santa Cruz, Santa Cruz, California 95064 – name: 4 Department of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, Los Angeles, California 90095 – name: 6 Departments of Neurology and Physiology, The David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California 90095 – name: 1 Molecular Biology Institute, University of California, Los Angeles, Los Angeles, California 90095 – name: 3 Department of Neuroscience, Tufts University School of Medicine, Boston, Massachusetts 02111 – name: 7 Howard Hughes Medical Institute, University of California, Los Angeles, Los Angeles, California 90095 – name: 2 Department of Biochemistry, School of Medicine, West Virginia University, Morgantown, West Virginia 26506 |
| Author_xml | – sequence: 1 givenname: Lauren T surname: Gehman fullname: Gehman, Lauren T organization: Molecular Biology Institute, University of California, Los Angeles, Los Angeles, California, USA – sequence: 2 givenname: Peter surname: Stoilov fullname: Stoilov, Peter organization: Department of Biochemistry, School of Medicine, West Virginia University – sequence: 3 givenname: Jamie surname: Maguire fullname: Maguire, Jamie organization: Department of Neuroscience, Tufts University School of Medicine – sequence: 4 givenname: Andrey surname: Damianov fullname: Damianov, Andrey organization: Department of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, Los Angeles, California, USA – sequence: 5 givenname: Chia-Ho surname: Lin fullname: Lin, Chia-Ho organization: Department of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, Los Angeles, California, USA – sequence: 6 givenname: Lily surname: Shiue fullname: Shiue, Lily organization: Department of Molecular, Cell and Developmental Biology, Sinsheimer Labs, University of California, Santa Cruz, Santa Cruz, California, USA – sequence: 7 givenname: Manuel surname: Ares fullname: Ares, Manuel organization: Department of Molecular, Cell and Developmental Biology, Sinsheimer Labs, University of California, Santa Cruz, Santa Cruz, California, USA – sequence: 8 givenname: Istvan surname: Mody fullname: Mody, Istvan organization: Department of Neurology, The David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California, USA., Department of Physiology, The David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California, USA – sequence: 9 givenname: Douglas L surname: Black fullname: Black, Douglas L email: dougb@microbio.ucla.edu organization: Molecular Biology Institute, University of California, Los Angeles, Los Angeles, California, USA., Department of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, Los Angeles, California, USA., Howard Hughes Medical Institute, University of California, Los Angeles |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24333647$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/21623373$$D View this record in MEDLINE/PubMed |
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| CODEN | NGENEC |
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| Snippet | The Rbfox family of RNA binding proteins mediate alternative splicing. Douglas Black and colleagues show that targeted deletion of the mouse
Rbfox1
gene in the... The Rbfox family of RNA binding proteins regulates alternative splicing of many important neuronal transcripts, but its role in neuronal physiology is not... The Rbfox family of RNA binding proteins regulates alternative splicing of many important neuronal transcripts but their role in neuronal physiology is not... |
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| SubjectTerms | 631/208/2489/144 631/337/1645/1946 692/699/375 Agriculture Alternative Splicing Animal Genetics and Genomics Animals Apoptosis Binding proteins Biological and medical sciences Biomarkers - metabolism Biomedical and Life Sciences Biomedicine Blotting, Western Brain - cytology Brain - metabolism Cancer Research Cell Proliferation Central nervous system Electrophysiology Female Fundamental and applied biological sciences. Psychology Gene Expression Profiling Gene Expression Regulation Gene Function Genetic aspects Genetics of eukaryotes. Biological and molecular evolution Homeostasis Human Genetics Human subjects Immunoenzyme Techniques Kainic Acid - toxicity letter Male Methods Mice Mice, Inbred C57BL Mice, Knockout Neurons - cytology Neurons - metabolism Oligonucleotide Array Sequence Analysis Physiological aspects Proteins Reverse Transcriptase Polymerase Chain Reaction RNA splicing RNA Splicing Factors RNA, Messenger - genetics RNA-Binding Proteins - physiology Rodents Seizures - chemically induced Synaptic Transmission |
| Title | The splicing regulator Rbfox1 (A2BP1) controls neuronal excitation in the mammalian brain |
| URI | https://link.springer.com/article/10.1038/ng.841 https://www.ncbi.nlm.nih.gov/pubmed/21623373 https://www.proquest.com/docview/880396612 https://www.proquest.com/docview/874186387 https://www.proquest.com/docview/883018495 https://pubmed.ncbi.nlm.nih.gov/PMC3125461 |
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