Paupar long non-coding RNA promotes KAP1 dependent chromatin changes and regulates olfactory bulb neurogenesis [CHIP-seq]
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ABSTRACT:
PROVIDER: PRJNA432593 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6685150_1.fastq.gz | Fastqsanger.gz | |||
| SRR6685150_2.fastq.gz | Fastqsanger.gz | |||
| SRR6685151_1.fastq.gz | Fastqsanger.gz | |||
| SRR6685151_2.fastq.gz | Fastqsanger.gz | |||
| SRR6685152_1.fastq.gz | Fastqsanger.gz |
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Project description:These data show that Paupar, a CNS expressed long non-coding RNA (lncRNA), directly and functionally associates with KAP1, an essential epigenetic regulatory protein. Transcriptome profiling of N2A cells identified 1,913 differentially expressed genes whose expression significantly changed (at a 5% false discovery rate [FDR]) greater than 1.4-fold (log2 fold change ≈ 0.5) upon KAP1 depletion. Examination of the intersection of KAP1 and Paupar transcriptional targets showed that Paupar and KAP1 control expression of a shared set of target genes that are enriched for regulators of neuronal function and cell cycle in N2A cells. Furthermore, CHART-seq and ChIP-seq derived Paupar-KAP1 genome-wide co-occupancy maps revealed a 4-fold enrichment of overlap between Paupar and KAP1 bound sequences on chromatin. This study also indicates that Paupar promotes KAP1 chromatin occupancy and H3K9me3 deposition at a subset of distal targets, through formation of a ribonucleoprotein complex containing Paupar, KAP1 and the PAX6 transcription factor. These observations provide important conceptual insights into the trans-acting modes of lncRNA-mediated epigenetic regulation and the mechanisms of KAP1 genomic recruitment.
2018-02-02 | GSE110032 | GEO
Project description:These data show that Paupar, a CNS expressed long non-coding RNA (lncRNA), directly and functionally associates with KAP1, an essential epigenetic regulatory protein. Transcriptome profiling of N2A cells identified 1,913 differentially expressed genes whose expression significantly changed (at a 5% false discovery rate [FDR]) greater than 1.4-fold (log2 fold change ≈ 0.5) upon KAP1 depletion. Examination of the intersection of KAP1 and Paupar transcriptional targets showed that Paupar and KAP1 control expression of a shared set of target genes that are enriched for regulators of neuronal function and cell cycle in N2A cells. Furthermore, CHART-seq and ChIP-seq derived Paupar-KAP1 genome-wide co-occupancy maps revealed a 4-fold enrichment of overlap between Paupar and KAP1 bound sequences on chromatin. This study also indicates that Paupar promotes KAP1 chromatin occupancy and H3K9me3 deposition at a subset of distal targets, through formation of a ribonucleoprotein complex containing Paupar, KAP1 and the PAX6 transcription factor. These observations provide important conceptual insights into the trans-acting modes of lncRNA-mediated epigenetic regulation and the mechanisms of KAP1 genomic recruitment.
2018-02-02 | GSE110031 | GEO
Project description:Paupar long non-coding RNA promotes KAP1 dependent chromatin changes and regulates olfactory bulb neurogenesis
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Project description:Neural stem cells (NSCs) in the subventricular zone (SVZ) produce functional neurons throughout life and are an accessible and robust system to understand neurodevelopmental mechanisms. Elucidating the properties of NSCs will also provide insights for their use in the treatment of neurodevelopmental disorders and brain injuries. However, the epigenetic mechanisms that maintain NSCs and control neurogenesis remain unclear. We previously showed that Paupar, a CNS-expressed long non-coding RNA (lncRNA), controls neuroblastoma cell growth by binding and modulating the activity of the KAP1 transcription co-factor. We interrogated the last stages of olfactory bulb (OB) neurogenesis and showed that depletion of these two molecules in vivo reduced the number of newborn neurons and delayed their morphological differentiation. Here we investigated upstream functions of these two epigenetic regulators in SVZ NSCs self-renewal and neurogenesis. We combined studies using inducible knockout and in vivo knockdown electroporation, with molecular analysis. Our results demonstrate that KAP1 and Paupar are broadly expressed in the normal postnatal/adult SVZ neurogenic lineage, that they physically interact in SVZ cells and regulate NSC behaviour in the SVZ. KAP1 directly maintains the neural stem cell pool and regulates the expression of genes involved in the cell cycle. Paupar, in turn maintains stem cell quiescence by restricting lineage progression from stem cells to transit amplifying progenitors (TAPs). These results suggest important roles for a KAP1-Paupar containing chromatin regulatory complex in the control of SVZ NSC and SVZ-OB neurogenesis.
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Project description:Neural stem cells (NSCs) in the subventricular zone (SVZ) produce functional neurons throughout life and are an accessible and robust system to understand neurodevelopmental mechanisms. Elucidating the properties of NSCs will also provide insights for their use in the treatment of neurodevelopmental disorders and brain injuries. However, the epigenetic mechanisms that maintain NSCs and control neurogenesis remain unclear. We previously showed that Paupar, a CNS-expressed long non-coding RNA (lncRNA), controls neuroblastoma cell growth by binding and modulating the activity of the KAP1 transcription co-factor. We interrogated the last stages of olfactory bulb (OB) neurogenesis and showed that depletion of these two molecules in vivo reduced the number of newborn neurons and delayed their morphological differentiation. Here we investigated upstream functions of these two epigenetic regulators in SVZ NSCs self-renewal and neurogenesis. We combined studies using inducible knockout and in vivo knockdown electroporation, with molecular analysis. Our results demonstrate that KAP1 and Paupar are broadly expressed in the normal postnatal/adult SVZ neurogenic lineage, that they physically interact in SVZ cells and regulate NSC behaviour in the SVZ. KAP1 directly maintains the neural stem cell pool and regulates the expression of genes involved in the cell cycle. Paupar, in turn maintains stem cell quiescence by restricting lineage progression from stem cells to transit amplifying progenitors (TAPs). These results suggest important roles for a KAP1-Paupar containing chromatin regulatory complex in the control of SVZ NSC and SVZ-OB neurogenesis.
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Project description:Paupar long non-coding RNA promotes KAP1 dependent chromatin changes and regulates olfactory bulb neurogenesis [gene expression]
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Project description:Many long non-coding RNAs (lncRNAs) are expressed during central nervous system (CNS) development, yet their in vivo roles and mechanisms of action remain poorly understood. Paupar, a CNS-expressed lncRNA, controls neuroblastoma cell growth by binding and modulating the activity of transcriptional regulatory elements in a genome-wide manner. We show here that the Paupar lncRNA directly binds KAP1, an essential epigenetic regulatory protein, and thereby regulates the expression of shared target genes important for proliferation and neuronal differentiation. Paupar promotes KAP1 chromatin occupancy and H3K9me3 deposition at a subset of distal targets, through the formation of a ribonucleoprotein complex containing Paupar, KAP1 and the PAX6 transcription factor. Paupar-KAP1 genome-wide co-occupancy reveals a fourfold enrichment of overlap between Paupar and KAP1 bound sequences, the majority of which also appear to associate with PAX6. Furthermore, both Paupar and Kap1 loss-of-function in vivo disrupt olfactory bulb neurogenesis. These observations provide important conceptual insights into the trans-acting modes of lncRNA-mediated epigenetic regulation and the mechanisms of KAP1 genomic recruitment, and identify Paupar and Kap1 as regulators of neurogenesis in vivo.
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Project description:Olfactory sensory neurons distinguish a large variety of odor molecules and direct the information through their axons to the olfactory bulb, the first site for the processing of olfactory information in the brain. Olfaction is very important for most mammals for the maintenance of a good quality of life. Accumulating evidences endorse that olfactory sensory decline is connected with neurodegenerative disorders including schizophrenia, depression, multiple sclerosis, Huntington's, Alzheimer's and Parkinson's diseases. For several decades, neuroanatomical, volumetric, and histological approaches have been the gold standard techniques employed to characterize the olfactory bulb functionality. Diagnosis and treatment of olfactory dysfunction remain significant health care challenges to society. Novel strategies and clues that assist in the identification of biomarker and drug development for aid in the prevention and cure of neurological diseases are necessary. However, little attention has been focused specifically on the molecular composition of the olfactory bulb from the perspective of proteomics. To this end, an in-depth mapping of the olfactory bulb proteome was carried out using high resolution tandem mass spectrometry, revealing a repertoire of 7,754 proteins. A large proportion of the identified proteins were predicted to be involved in diverse biological processes including signal transduction, metabolism, transport, olfaction and protein synthesis. Pathway analysis of the identified proteins shows that, these proteins are predominantly involved in metabolic and neural processes, chromatin modeling, and synaptic vesicle transport associated with neuronal transmission. In total, our study offers valuable understandings into the molecular composition of the human olfactory bulb proteome that could possibly help neuroscience community to understand the olfactory bulb better and open avenues for intervention strategies for olfactory dysfunction in the future.
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