Project description:We created a mutator protein. The mutator, was prepared by fusing a PmCDA1 (Petromyzon marinus Cytidine DeAminase) and E.coli RNA polymerase alpha subunit(EcoRNAP alpha). After 120 cycles, whole genome sequencing was performed on the wild type and evolved sample. After characterization of the mutation capacity of our mutator, we evolved a sucrose utilization strain and we sequenced Suc strain.
Project description:We used bisulfite conversion and Illumina sequencing to analyse miR-150 DNA methylation pattern lost in cells treated with decitabine, a demethylating agent, Crizotinib, an inhibitor of of ALK activity or siALK Targeted bisulfite conversion and Illumina sequencing in two cell lines bearing the t(2;5)(p23;q35)
Project description:We have performed RNA sequencing on kidneys from inclusion body nephropathy-affected mice and compared the data to healthy, uninfected controls. Using a metagenomics approach, we report the identification of the disease causing agent as an atypical virus, mouse kidney parvovirus (MKPV), belonging to a divergent genus of the Parvoviridae. The RNA sequencing also enabled us to assess the host response to MKPV-infection.
Project description:Influenza is a major cause of morbidity and mortality worldwide, and the emerging drug resistance poses an increasing challenge to the treatment of influenza virus infection. Therefore, the development of a novel antiviral drugs has become an urgent task to combat against the influenza viruses that are resistant to the current therapeutic treatment. Here, by screening a small molecule chemical compound library, we identified 3-anhydro-6-epi-ophiobolin A (named L435) as a potent anti-influenza agent. Mechanistically, L435 markedly reduced influenza virus replication in vitro and in vivo. Importantly, L435 treatment improved the survival of influenza-virus-infected mice, suggesting that L435 may be a novel therapeutic agent for treatment of influenza virus infections. This microarray experiment was carried out to explore gene expression changes in influenza-virus-infected A549 cells after L435 treatment, and find out why L435 could inhibit the replication of influenza A virus.
Project description:<p>Algal blooms drive global biogeochemical cycles of key nutrients in the oceans and serve as hotspots for biological interactions. The massive spring blooms of the cosmopolitan coccolithophore <em>Emiliania huxleyi </em>(<em>E. huxleyi</em>) are often infected by the lytic <em>Emiliania huxleyi</em> specific virus (EhV) which is a major mortality agent triggering bloom demise. Nonetheless, the multi-annual 'boom and bust' pattern of<em> E. huxleyi</em> suggests that mechanisms of coexistence are essential for these host-virus dynamics. To investigate host-virus coexistence, we developed a new model system from an <em>E. huxleyi</em> culture which recovered from viral infection. The recovered population coexists with the virus, as host cells continue to grow in parallel to viral production. By applying a single-molecule fluorescence in situ hybridization (smFISH) approach to quantify the fraction of infected cells and assessing infection-specific lipid biomarkers, we identified a small subpopulation (5-7% of cells) that was infected and produced new virions, whereas the majority of the host population could resist infection. To further assess population heterogeneity, we generated monoclonal strain collections using single-cell sorting and subsequently phenotyped their susceptibility to EhV infection. This unraveled a substantial cell-to-cell heterogeneity across a continuum of susceptibility to resistance, suggesting that infection outcomes may vary depending on the individual cell. These results add a new dimension to our understanding of the complexity of host-virus interactions that are commonly assessed in bulk and described by binary definitions of resistance or susceptibility. We propose that phenotypic heterogeneity drives <em>E. huxleyi-</em>EhV coexistence and may potentially provide the coexisting strain an ecological advantage by killing competing susceptible strains.</p>