Ontology highlight
ABSTRACT:
PROVIDER: PRJNA517593 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8512260.fastq.gz | Fastqsanger.gz | |||
| SRR8512261.fastq.gz | Fastqsanger.gz | |||
| SRR8512262.fastq.gz | Fastqsanger.gz | |||
| SRR8512263.fastq.gz | Fastqsanger.gz | |||
| SRR8512264.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 8 |
Similar Datasets
Project description:Paramyxoviruses are negative sense single-stranded RNA viruses that comprise many important human and animal pathogens, including human parainfluenza viruses. These viruses bud from the plasma membrane of infected cells after the viral ribonucleoprotein complex (vRNP) is transported from the cytoplasm to the cell membrane via Rab11a marked recycling endosomes. The viral proteins that are critical for mediating this important initial step in viral assembly are unknown. Here we use the model paramyxovirus, murine parainfluenza virus 1, or Sendai virus (SeV), to investigate the roles of viral proteins in Rab11a-driven virion assembly. We previously reported that infection with SeV containing high levels of copy-back defective viral genomes (DVGs) generates heterogenous populations of cells, with cells enriched in full-length virus producing viral particles containing standard or defective viral genomes, while cells enriched in DVGs did not, despite high levels of defective viral genome replication. Here we take advantage of this heterogenous cell phenotype to identify proteins that mediate interaction of vRNPs with Rab11a. We examine the role of matrix protein and nucleoprotein and determine that they are not sufficient to drive interaction of vRNPs and recycling endosomes. Then, using a combination of mass spectrometry and comparative protein abundance and localization in DVG- and FL-high cells, we identify viral polymerase complex components L and, specifically, its cofactor C proteins as interactors with Rab11a. We find that accumulation of these proteins within the cell is the defining feature that differentiates cells that proceed to viral egress from cells which remain in replication phases. Paramyxoviruses are a family of viruses that include a number of pathogens with significant burdens on human health. Particularly, human parainfluenza viruses are an important cause of pneumonia and bronchiolitis in children and do not have any vaccines or direct acting antivirals. These cytoplasmic replicating viruses bud from the plasma membrane and coopt cellular endosomal recycling pathways to traffic viral ribonucleoprotein complexes from the cytoplasm to the membrane of infected cells, yet the viral proteins required for viral engagement with the recycling endosome pathway is not known. Here we use the model paramyxovirus Sendai virus, or murine parainfluenza virus 1, to investigate the role of viral proteins in this initial step in viral assembly. We find that viral polymerase components large protein L and accessory C proteins are necessary for engagement with recycling endosomes. These findings are important in identifying viral targets for the development of antivirals.
2020-08-06 | PXD019637 | Pride
Project description:Comparison of Mutations in Human Parainfluenza Viruses during Passage
| PRJDB18043 | ENA
Project description:High throughput sequencing of small RNAs (mature miRNA and piRNA/piRNA-like molecules) from control- and sporadic Parkinson´s disease patient derived fibroblasts (n=15), induced pluripotent stem cells (n=26) and differentiated midbrain neurons (n=10). In parallel, cingulate gyrus samples from eight control- and eight Parkinson´s disease patients obtained from the Netherlands Brain Bank were sequenced. We found significant differences between the groups in every cell type and in tissue.
2018-10-08 | GSE110719 | GEO
Project description:Human parainfluenza virus 1 Genome Sequencing
| PRJNA73053 | ENA
Project description:Human parainfluenza virus 3 Genome Sequencing
| PRJNA73055 | ENA
Project description:Life-threatening pulmonary influenza can be caused by inborn errors of type I and III IFN immunity. We report a 5 year-old child with severe pulmonary influenza at 2 years. She is homozygous for a loss-of-function IRF9 allele. Her cells activate gamma-activated factor (GAF) STAT1 homodimers but not interferon-stimulated gene factor 3 (ISGF3) trimers (STAT1/STAT2/IRF9) in response to IFN-α2b. The transcriptome induced by IFN-α2b in the patient’s cells is much narrower than that of control cells; however, induction of a subset of interferon-stimulated gene transcripts remains detectable. In vitro, the patient’s cells do not control three respiratory viruses, influenza A virus (IAV), parainfluenza virus, and respiratory syncytial virus. These phenotypes are rescued by wild-type IRF9, whereas silencing IRF9 expression in control cells increases viral replication. However, the child has controlled various common viruses in vivo, including respiratory viruses other than IAV. Our findings show that human IRF9- and ISGF3-dependent type I and III IFN responsive pathways are essential for controlling IAV.
2018-08-06 | GSE117637 | GEO
Project description:Enhancers are non-coding genomic features that regulate the transcriptional output of their target genes. Their dysregulation has been associated with various diseases including cancer. However, identification and characterisation of non-coding mutations that are relevant for tumorigenesis and prognosis remain a major challenge. Here we present the detection and characterisation of enhancer mutations in a genome-wide analysis of three lung cancer subtypes. We carefully define lung tissue-specific enhancers across the genome by integrating novel experimental data and reference public datasets of epigenomic signatures from eight lung cell lines and primary tissue. We observe that in lung cancer, the mutation burden at enhancers and exons is similar, whereas their corresponding mutation signatures show stark differences. Our results indicate that recurrent mutations in individual enhancers significantly impact the expression of target genes with potential relevance for prognosis. We also demonstrate that the genes enriched for mutated enhancers recurrently converge on the regulation of key biological process and pathways.
2023-09-27 | GSE228831 | GEO
Project description:Enhancers are non-coding genomic features that regulate the transcriptional output of their target genes. Their dysregulation has been associated with various diseases including cancer. However, identification and characterisation of non-coding mutations that are relevant for tumorigenesis and prognosis remain a major challenge. Here we present the detection and characterisation of enhancer mutations in a genome-wide analysis of three lung cancer subtypes. We carefully define lung tissue-specific enhancers across the genome by integrating novel experimental data and reference public datasets of epigenomic signatures from eight lung cell lines and primary tissue. We observe that in lung cancer, the mutation burden at enhancers and exons is similar, whereas their corresponding mutation signatures show stark differences. Our results indicate that recurrent mutations in individual enhancers significantly impact the expression of target genes with potential relevance for prognosis. We also demonstrate that the genes enriched for mutated enhancers recurrently converge on the regulation of key biological process and pathways.
2023-09-27 | GSE228830 | GEO
Project description:Here we aim to demonstrate a novel approach enabling standardised and rapid characterisation of transplanted xenografts in the rodent brain. The approach employs bulk tissue dissection, inclusive of the grafted human cells and surrounding host (rodent) tissue, and utilises differences in the RNA sequences between the species to discriminate the xenograft from host gene expression. To demonstrate and validate this technique, we assessed grafts of undifferentiated human stem cells, immature neural progenitors and mature neurons following transplantation into the rodent brain. Mixed species RNAseq was conducted on the bulk dissected tissue, and a high stringency analysis pipeline developed to discriminate the human reads. Xenograft-specific RNAseq allowed accurate profiling the complete transcriptome of the transplant with high sensitivity and accuracy. The profile allowed the identification of novel gene expression and an unbiased characterisation of graft composition, providing a valuable tool for the analysis of xenografts. This characterisation will be especially crucial for the characterisation of grafts in pre-clinical and batch testing of therapeutic cell preparations prior to translation to the clinic.
2019-08-31 | GSE126804 | GEO