Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1199045 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31781121_1.fastq.gz | Fastqsanger.gz | |||
| SRR31781121_2.fastq.gz | Fastqsanger.gz | |||
| SRR31781122_1.fastq.gz | Fastqsanger.gz | |||
| SRR31781122_2.fastq.gz | Fastqsanger.gz | |||
| SRR31781123_1.fastq.gz | Fastqsanger.gz |
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Project description:Many annotated long noncoding RNAs (lncRNAs) contain small open reading frames (sORFs), some of which have been demonstrated to encode small proteins or micropeptides with fundamental biological importance. However, the small proteins or micropeptides encoded by lncRNAs and their functions in viral infection remain largely unexplored. Here, we identified and characterized a small 110-amino acid protein named ORF6 encoded by the putative lncRNA PCBP1-AS1. Interestingly, both PCBP1-AS1 and ORF6 were significantly upregulated by influenza virus infection. Furthermore, we observed that they were markedly induced by type I interferon treatment. Overexpression of PCBP1-AS1 or ORF6 enhanced influenza virus replication. Conversely, knockdown of PCBP1-AS1 or knockout of ORF6 inhibited the viral production. In addition, loss-of-function experiment demonstrated that ORF6 is essential for PCBP1-AS1 to facilitate influenza virus replication. Importantly, the overexpression of ORF6 induced enhancement of autophagy by increasing the expression of ATG7, a gene encoding an essential effector enzyme for canonical autophagy. These findings reveal a lncRNA-derived small protein that is exploited by influenza virus, and provide new insights into the virus-host regulatory network.
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Project description:Small, compact genomes confer a selective advantage to viruses, yet human cytomegalovirus (HCMV) expresses the long non-coding RNAs (lncRNAs) RNA1.2, RNA2.7, RNA4.9, and RNA5.0. These lncRNAs account for majority of the viral transcriptome, but their functions remain largely unknown. Here, we showed that HCMV lncRNAs, except for RNA5.0, are required throughout the entire viral life cycle. Deletion of each lncRNA resulted in a decrease in viral progeny during lytic replication and failing to efficiently establish latent reservoirs and reactivate. Nanopore direct RNA sequencing of native lncRNA molecules revealed that each lncRNA exhibited a dynamic modification landscape, depending on the state of infection. Global analysis of the lncRNA interactome identified 32, 11, and 89 host factors that specifically bind to RNA1.2, RNA2.7, and RNA4.9, respectively. Moreover, 52 proteins commonly bound to the three lncRNAs were identified, including 11 antiviral immunity-related proteins. Our molecular analyses found that three lncRNAs are modified with N⁶-methyladenosine (m6A) and interact with m6A readers in all infection states. In-depth functional analysis revealed that m6A–mediated lncRNA stabilization as the key mechanism by which lncRNAs are maintained at high levels. Our study lays the groundwork for understanding viral lncRNA–mediated regulation of host-virus interaction throughout the HCMV life cycle.
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Project description:A large number of lncRNAs has been found aberrant expression in breast cancer and paly functional role in tumor progression. However, the role of small peptide hidden in lncRNA are largely unexplored. In this study, we applied the CRISPR/Cas9 screen and ribosome profiling to systematically discover nocanonical open reading frame encoded in long noncoding RNAs (lncRNAs) and explored their critical roles in ER+ breast cancer.
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Project description:Many annotated long noncoding RNAs (lncRNAs) contain small open reading frames (sORFs), some of which have been demonstrated to encode small proteins or micropeptides with fundamental biological importance. While the small proteins or micropeptides hidden in lncRNA are gradually being revealed, their functions in influenza virus infection remain largely unexplored. Here, we identified and characterized a small 110-amino acid protein named PAESP that is encoded by the putative lncRNA PCBP1-AS1. We found that both PCBP1-AS1 and PAESP were upregulated by influenza virus infection as well as type I interferon treatment. Overexpression of PCBP1-AS1 or PAESP enhanced influenza virus replication. Conversely, knockdown of PCBP1-AS1 or knockout of PAESP inhibited viral production. In addition, loss-of-function experiment demonstrated that PAESP is essential for PCBP1-AS1 to facilitate influenza virus replication. More importantly, the overexpression of PAESP increases the mRNA level of several genes such as IFIT2 and IFIT3, which have been proved to be retasked by influenza virus from canonical antiviral factors into proviral effectors. Interestingly, when IFIT2 or IFIT3 expression was knocked down in PAESP-overexpressed cells, the virus titers significantly decreased compared to control cells. These findings reveal a novel lncRNA-derived small protein that is exploited by influenza virus and provide new insights into the virus-host regulatory network.
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Project description:Long non-coding RNAs are frequently associated with broad modulation of gene expression and thus provide the cell with the ability to synchronize entire metabolic processes. We used transcriptomic and proteomic approaches to investigate whether the most abundant human cytomegalovirus-encoded lncRNA, RNA2.7, has this characteristic. By comparing RNA2.7 deletion mutants with wild-type virus, RNA2.7 was found to regulate a large number of cellular genes late in infection. Pathway analysis indicated that >100 RNA2.7-regulated cellular genes are associated with promoting cell movement, and ten of the most highly regulated were verified in further experiments. Morphological analysis and live cell tracking showed that RNA2.7 promotes the movement and detachment of infected cells late in infection, and plaque assays using sparse cell monolayers demonstrated that RNA2.7 promotes cell-to-cell dissemination and spread of virus. Bioinformatic analysis indicated that RNA2.7-upregulated mRNAs are relatively A+U-rich, which is a trait associated with transcript instability, and that they are also enriched in motifs associated with mRNA instability. Experiments involving transcriptional inhibition showed that transcripts from four RNA2.7-regulated cellular genes were longer-lived in the presence of RNA2.7. These findings demonstrate that RNA2.7 promotes cell movement and viral dissemination late in infection and indicate that this may be due to general stabilization of A+U-rich transcripts.
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Project description:Viruses are known for their extremely compact genomes composed almost entirely of protein-coding genes. Nonetheless, four long noncoding RNAs (lncRNAs) are encoded by human cytomegalovirus (HCMV). Although these RNAs accumulate to high levels during lytic infection, their functions remain largely unknown. Here, we show that HCMV-encoded lncRNA4.9 localizes to the viral nuclear replication compartment, and that its depletion restricts viral DNA replication and viral growth. RNA4.9 is transcribed from the HCMV origin of replication (oriLyt) and forms an RNA-DNA hybrid (R-loop) through its G+C-rich 5’ end, and this may be important for the initiation of viral DNA replication. Furthermore, interference with RNA4.9 expression drastically reduces the levels of the viral single-stranded DNA-binding protein (ssDBP), and overexpression of ssDBP alleviates the inhibition of viral DNA replication and growth caused by RNA4.9 depletion. We also identified a similar, oriLyt-embedded, G+C-rich lncRNA in murine cytomegalovirus (MCMV). Knockdown of this lncRNA interferes with MCMV ssDBP expression and viral DNA replication. These results indicate that HCMV RNA4.9 plays an important role in regulating viral DNA replication by coupling oriLyt activity to ssDBP levels, and that this novel activity may be conserved in other betaherpesviruses.
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2015-11-04 | GSE74610 | GEO
Project description:To test the hypothesis that circRNAs might encode functional peptides in mammalian cells, we studied the long intergenic non-protein coding RNA, p53 induced transcript (LINC-PINT), which was previously reported as a tumor suppressor and connected p53 activation with polycomb repressive complex 2 (PRC2). We selected this long noncoding RNA (lncRNA) for further analysis because LINC-PINT has a long exon 2 which in accordance with the bioinformatical analyzed circular RNA standard.The following immunoblotting showed 87aa peptide level also decreased, indicating that this peptide is encoded by circPINTexon2. We name this circRNA encoded peptide PINT87aa. To investigate the possible regulatory role of PINT87aa, we did the expression micro array in PINT87aa stably transfect U251 or U87 glioblastoma cells and their control cells. The array analysis reveals that PINT87aa may involve in the cell cycle regulation, anti-apoptosis effects and multiple oncogenic signaling pathway activation.
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