Dataset Information

Identification of a host protein interacting with Tomato spotted wilt virus ribonucleoproteins from Nicotiana benthamiana and yeast.

ABSTRACT: Viruses are obligate intracellular pathogens that depend on host factors to complete their infection cycle. Very little is known of which plant factors are required for successful Tomato spotted wilt orthotospovirus (TSWV) infection. The viral ribonucleoprotein (RNP) fraction from TSWV infected Nicotiana benthamiana plants was purified and its protein composition was analysed by proteomics by mass spectrometry to identify host proteins that co-purify with viral RNPs. Related, we expressed a TSWV replicon system in a non-host system, Bakers’ yeast (Saccharomyces cerevisiae), and purified as well the RNP fraction from yeast. Comparative proteomics was used to find common enriched proteins observed in both yeast and plant RNP fractions.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Nicotiana Benthamiana Tomato Spotted Wilt Tospovirus Saccharomyces Cerevisiae (baker's Yeast)

SUBMITTER: Sjef Boeren

LAB HEAD: Sjef Boeren

PROVIDER: PXD026246 | Pride | 2021-11-10

REPOSITORIES: Pride

ACCESS DATA

Publications

An Isoform of the Eukaryotic Translation Elongation Factor 1A (eEF1a) Acts as a Pro-Viral Factor Required for Tomato Spotted Wilt Virus Disease in <i>Nicotiana benthamiana</i>.

Helderman Tieme A TA Deurhof Laurens L Bertran André A Boeren Sjef S Fokkens Like L Kormelink Richard R Joosten Matthieu H A J MHAJ Prins Marcel M van den Burg Harrold A HA

Viruses 20211030 11

The tripartite genome of the negative-stranded RNA virus <i>Tomato spotted wilt orthotospovirus</i> (TSWV) is assembled, together with two viral proteins, the nucleocapsid protein and the RNA-dependent RNA polymerase, into infectious ribonucleoprotein complexes (RNPs). These two viral proteins are, together, essential for viral replication and transcription, yet our knowledge on the host factors supporting these two processes remains limited. To fill this knowledge gap, the protein composition o ...[more]

PMID: 34834996

Similar Datasets

Project description:MicroRNAs (miRNAs) repress the expression levels of genes by binding to mRNA transcripts, acting as master regulators of cellular processes. Differential expression of miRNAs has been linked to viral-associated diseases involving members of the hepacivirus, herpesvirus, and retrovirus families. In contrast, limited biological and molecular information has been reported on the potential role of cellular miRNAs in the lifecycle of influenza A viruses (infA). In this study, we hypothesize that elucidating the miRNA expression signatures induced by low-pathogenic swine-origin influenza A virus (S-OIV) pandemic H1N1 (2009) and highly pathogenic avian-origin (A-OIV) H7N7 (2003) infections could reveal temporal and strain-specific miRNA fingerprints during the viral lifecycle, shedding important insights into the potential role of cellular miRNAs in host-infA interactions. Using a microfluidic microarray platform, we profiled cellular miRNA expression in human A549 cells infected with S- and A-OIVs at multiple time-points during the viral lifecycle, including global gene expression profiling during S-OIV infection. Using target prediction and pathway enrichment analyses, we identified the key cellular pathways associated with the differentially expressed miRNAs and predicted mRNA targets during infA infection, including immune system, cell proliferation, apoptosis, cell cycle, and DNA replication and repair. By identifying the specific and dynamic molecular phenotypic changes (microRNAome) triggered by S- and A-OIV infection in human cells, we provide experimental evidence demonstrating a series of temporal- and strain-specific host molecular responses involving different combinatorial contributions of multiple cellular miRNAs. Our results also identify novel potential exosomal miRNA biomarkers associated with pandemic S-OIV and deadly A-OIV-host infection. Control (mock-infected) samples: 12 (2 technical replicates, averaged), Infected samples: 6, for each time-point (0, 4, 8, 24, 48 and 72 hours post infection). The experiment was performed in six replicates.

Project description:MicroRNAs (miRNAs) repress the expression levels of genes by binding to mRNA transcripts, acting as master regulators of cellular processes. Differential expression of miRNAs has been linked to viral-associated diseases involving members of the hepacivirus, herpesvirus, and retrovirus families. In contrast, limited biological and molecular information has been reported on the potential role of cellular miRNAs in the lifecycle of influenza A viruses (infA). In this study, we hypothesize that elucidating the miRNA expression signatures induced by low-pathogenic swine-origin influenza A virus (S-OIV) pandemic H1N1 (2009) and highly pathogenic avian-origin (A-OIV) H7N7 (2003) infections could reveal temporal and strain-specific miRNA fingerprints during the viral lifecycle, shedding important insights into the potential role of cellular miRNAs in host-infA interactions. Using a microfluidic microarray platform, we profiled cellular miRNA expression in human A549 cells infected with S- and A-OIVs at multiple time-points during the viral lifecycle, including global gene expression profiling during S-OIV infection. Using target prediction and pathway enrichment analyses, we identified the key cellular pathways associated with the differentially expressed miRNAs and predicted mRNA targets during infA infection, including immune system, cell proliferation, apoptosis, cell cycle, and DNA replication and repair. By identifying the specific and dynamic molecular phenotypic changes (microRNAome) triggered by S- and A-OIV infection in human cells, we provide experimental evidence demonstrating a series of temporal- and strain-specific host molecular responses involving different combinatorial contributions of multiple cellular miRNAs. Our results also identify novel potential exosomal miRNA biomarkers associated with pandemic S-OIV and deadly A-OIV-host infection. Control (mock-infected) samples: 12, Infected samples: 6, for each time-point (0, 4, 8, 24, 48 and 72 hours post infection). Seven replicates for each miRNA were found on the microarray chips, for which the median has been retained. The experiment was performed in six replicates.

Project description:MicroRNAs (miRNAs) repress the expression levels of genes by binding to mRNA transcripts, acting as master regulators of cellular processes. Differential expression of miRNAs has been linked to viral-associated diseases involving members of the hepacivirus, herpesvirus, and retrovirus families. In contrast, limited biological and molecular information has been reported on the potential role of cellular miRNAs in the lifecycle of influenza A viruses (infA). In this study, we hypothesize that elucidating the miRNA expression signatures induced by low-pathogenic swine-origin influenza A virus (S-OIV) pandemic H1N1 (2009) and highly pathogenic avian-origin (A-OIV) H7N7 (2003) infections could reveal temporal and strain-specific miRNA fingerprints during the viral lifecycle, shedding important insights into the potential role of cellular miRNAs in host-infA interactions. Using a microfluidic microarray platform, we profiled cellular miRNA expression in human A549 cells infected with S- and A-OIVs at multiple time-points during the viral lifecycle, including global gene expression profiling during S-OIV infection. Using target prediction and pathway enrichment analyses, we identified the key cellular pathways associated with the differentially expressed miRNAs and predicted mRNA targets during infA infection, including immune system, cell proliferation, apoptosis, cell cycle, and DNA replication and repair. By identifying the specific and dynamic molecular phenotypic changes (microRNAome) triggered by S- and A-OIV infection in human cells, we provide experimental evidence demonstrating a series of temporal- and strain-specific host molecular responses involving different combinatorial contributions of multiple cellular miRNAs. Our results also identify novel potential exosomal miRNA biomarkers associated with pandemic S-OIV and deadly A-OIV-host infection. Control (mock-infected) samples: 12, Infected samples: 6, for each time-point (0, 4, 8, 24, 48 and 72 hours post infection). Seven replicates for each miRNA were found on the microarray chips, for which the median has been retained. The experiment was performed in six replicates. The H1N1 RNA in the mock-infected samples in chip 1 and the hour 4 samples in chip 2 were found to be degraded during the mRNA profiling; therefore, they were excluded from the statistical analysis.

Dataset Information

Identification of a host protein interacting with Tomato spotted wilt virus ribonucleoproteins from Nicotiana benthamiana and yeast.

Publications

An Isoform of the Eukaryotic Translation Elongation Factor 1A (eEF1a) Acts as a Pro-Viral Factor Required for Tomato Spotted Wilt Virus Disease in <i>Nicotiana benthamiana</i>.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure