The RNA-binding protein Sfpq regulates long neuronal genes in transcriptional elongation
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA257815 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1539410.fastq.gz | Fastqsanger.gz | |||
| SRR1539411.fastq.gz | Fastqsanger.gz | |||
| SRR1539412.fastq.gz | Fastqsanger.gz | |||
| SRR1539413.fastq.gz | Fastqsanger.gz | |||
| SRR1539414.fastq.gz | Fastqsanger.gz |
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Project description:Mammalian neurons express extra-long pre-mRNAs which are vulnerable to misregualtion of transcriptional elongation or processing but their regulation is still largely unknown. Here we found that RNA-binding protein PSF is specifically expressed in differentiated neuron of embryonic mouse brain and is essential for the expression of extra-long neuronal gene. HITS-CLIP indicated co-transcriptional binding of PSF to the nascent pre-mRNAs. When PSF was disrupted, pre-mRNA level of long genes was down-regulated in the middle of their transcripts toward their 3’ ends. In Pol II ChIP-Seq, decrease of the RNA polymerase II density was observed parallel to pre-mRNAs, indicating that transcriptional elongation was impaired. Loss of PSF caused massive apoptosis in embryonic mouse brains and heterozygous PSF mutant mice displayed schizophrenia-like abnormal behaviors. Gene Ontology analysis demonstrated that PSF-regulated genes have essential functions at the late developmental stage of brains. Our findings indicate that PSF is required for the neuronal development through facilitating the transcriptional elongation of extra-long neuronal genes and dysfunction of PSF could be a cause of neurodevelopmental and psychiatric disorders.
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Project description:Mammalian neurons express extra-long pre-mRNAs which are vulnerable to misregualtion of transcriptional elongation or processing but their regulation is still largely unknown. Here we found that RNA-binding protein PSF is specifically expressed in differentiated neuron of embryonic mouse brain and is essential for the expression of extra-long neuronal gene. HITS-CLIP indicated co-transcriptional binding of PSF to the nascent pre-mRNAs. When PSF was disrupted, pre-mRNA level of long genes was down-regulated in the middle of their transcripts toward their 3’ ends. In Pol II ChIP-Seq, decrease of the RNA polymerase II density was observed parallel to pre-mRNAs, indicating that transcriptional elongation was impaired. Loss of PSF caused massive apoptosis in embryonic mouse brains and heterozygous PSF mutant mice displayed schizophrenia-like abnormal behaviors. Gene Ontology analysis demonstrated that PSF-regulated genes have essential functions at the late developmental stage of brains. Our findings indicate that PSF is required for the neuronal development through facilitating the transcriptional elongation of extra-long neuronal genes and dysfunction of PSF could be a cause of neurodevelopmental and psychiatric disorders.
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Project description:Mammalian neurons express extra-long pre-mRNAs which are vulnerable to misregualtion of transcriptional elongation or processing but their regulation is still largely unknown. Here we found that RNA-binding protein PSF is specifically expressed in differentiated neuron of embryonic mouse brain and is essential for the expression of extra-long neuronal gene. HITS-CLIP indicated co-transcriptional binding of PSF to the nascent pre-mRNAs. When PSF was disrupted, pre-mRNA level of long genes was down-regulated in the middle of their transcripts toward their 3’ ends. In Pol II ChIP-Seq, decrease of the RNA polymerase II density was observed parallel to pre-mRNAs, indicating that transcriptional elongation was impaired. Loss of PSF caused massive apoptosis in embryonic mouse brains and heterozygous PSF mutant mice displayed schizophrenia-like abnormal behaviors. Gene Ontology analysis demonstrated that PSF-regulated genes have essential functions at the late developmental stage of brains. Our findings indicate that PSF is required for the neuronal development through facilitating the transcriptional elongation of extra-long neuronal genes and dysfunction of PSF could be a cause of neurodevelopmental and psychiatric disorders.
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Project description:Mammalian neurons express extra-long pre-mRNAs which are vulnerable to misregualtion of transcriptional elongation or processing but their regulation is still largely unknown. Here we found that RNA-binding protein PSF is specifically expressed in differentiated neuron of embryonic mouse brain and is essential for the expression of extra-long neuronal gene. HITS-CLIP indicated co-transcriptional binding of PSF to the nascent pre-mRNAs. When PSF was disrupted, pre-mRNA level of long genes was down-regulated in the middle of their transcripts toward their 3’ ends. In Pol II ChIP-Seq, decrease of the RNA polymerase II density was observed parallel to pre-mRNAs, indicating that transcriptional elongation was impaired. Loss of PSF caused massive apoptosis in embryonic mouse brains and heterozygous PSF mutant mice displayed schizophrenia-like abnormal behaviors. Gene Ontology analysis demonstrated that PSF-regulated genes have essential functions at the late developmental stage of brains. Our findings indicate that PSF is required for the neuronal development through facilitating the transcriptional elongation of extra-long neuronal genes and dysfunction of PSF could be a cause of neurodevelopmental and psychiatric disorders.
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Project description:Mammalian neurons express extra-long pre-mRNAs which are vulnerable to misregualtion of transcriptional elongation or processing but their regulation is still largely unknown. Here we found that RNA-binding protein PSF is specifically expressed in differentiated neuron of embryonic mouse brain and is essential for the expression of extra-long neuronal gene. HITS-CLIP indicated co-transcriptional binding of PSF to the nascent pre-mRNAs. When PSF was disrupted, pre-mRNA level of long genes was down-regulated in the middle of their transcripts toward their 3’ ends. In Pol II ChIP-Seq, decrease of the RNA polymerase II density was observed parallel to pre-mRNAs, indicating that transcriptional elongation was impaired. Loss of PSF caused massive apoptosis in embryonic mouse brains and heterozygous PSF mutant mice displayed schizophrenia-like abnormal behaviors. Gene Ontology analysis demonstrated that PSF-regulated genes have essential functions at the late developmental stage of brains. Our findings indicate that PSF is required for the neuronal development through facilitating the transcriptional elongation of extra-long neuronal genes and dysfunction of PSF could be a cause of neurodevelopmental and psychiatric disorders.
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Project description:Growing evidences are suggesting that extra-long genes in mammals are vulnerable for full-gene length transcription and dysregulation of long genes is a mechanism underlying human genetic disorders. Skeletal muscle expresses Dystrophin which is 2.26 Mbp in length; however, how long-distance transcription is achieved is totally unknown. We had discovered RNA-binding protein SFPQ preferentially binds to long pre-mRNAs and specifically regulates the cluster of neuronal genes > 100 kbp. Here we investigated the roles of SFPQ for long gene expression, target specificities, and also physiological functions in skeletal muscle. Loss of Sfpq selectively downregulated genes >100 kbp including Dystrophin and caused progressive muscle mass reduction and metabolic myopathy characterized by glycogen accumulation and decreased abundance of mitochondrial oxidative phosphorylation complexes. Functional clustering analysis identified metabolic pathway related genes as the targets of SFPQ. These findings indicate target gene specificities and tissue-specific physiological functions of SFPQ in skeletal muscle.
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Project description:Growing evidences are suggesting that extra-long genes in mammals are vulnerable for full-gene length transcription and dysregulation of long genes is a mechanism underlying human genetic disorders. Skeletal muscle expresses Dystrophin which is 2.26 Mbp in length; however, how long-distance transcription is achieved is totally unknown. We had discovered RNA-binding protein SFPQ preferentially binds to long pre-mRNAs and specifically regulates the cluster of neuronal genes > 100 kbp. Here we investigated the roles of SFPQ for long gene expression, target specificities, and also physiological functions in skeletal muscle. Loss of Sfpq selectively downregulated genes >100 kbp including Dystrophin and caused progressive muscle mass reduction and metabolic myopathy characterized by glycogen accumulation and decreased abundance of mitochondrial oxidative phosphorylation complexes. Functional clustering analysis identified metabolic pathway related genes as the targets of SFPQ. These findings indicate target gene specificities and tissue-specific physiological functions of SFPQ in skeletal muscle.
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