Project description:Perkinsus marinus is an intracellular parasitic protozoan that is responsible for serious disease epizootics in marine bivalve molluscs worldwide and along with P. olseni belongs to the OIE list of notified diseases. Despite all available information on P. marinus genomics, more baseline data is required at the proteomic level for a better understanding of P. marinus biological processes, including virulence mechanisms. In the present study, we have established in vitro clonal cultures of P. marinus from infected gills and mantle tissues of C. rhizophorae to evaluate the parasite cellular proteomic profile. A high throughput label-free shotgun HDMS approach using nanoUPLC-MS was used. Our intention was to provide the first comprehensive proteome profile of P. marinus that might serve as a valuable resource for future investigations involving comparative analyses of P. marinus from different regions, as well as comparisons of different species of Perkinsus.
Project description:To investigate the virological properties of SARS-CoV-2 variants, we amplified the clinical isolates of an early pandemic D614G-bearing isolate (B.1.1 lineage, strain TKYE610670; GISAID ID: EPI_ISL_479681), a Delta isolate (B.1.617.2 lineage, strain TKYTK1734; GISAID ID: EPI_ISL_2378732) and an Omicron isolate (BA.1 lineage, strain TY38-873; GISAID ID: EPI_ISL_7418017) and prepared the working viruses.
Project description:A circadian gene expression study in model marine cyanobacteria Prochlorococcus marinus MED4 was performed in order to evaluate circadian gene expression and identify genes which were regulated dependent on circadian photoperiod or light intensity.
Project description:Unscheduled R-loops are a major source of replication stress and DNA damage. R-loop-induced replication defects are sensed and suppressed by ATR kinase, whereas it is not known whether R-loop itself is actively involved in ATR activation and, if so, how this is achieved. Here, we report that the nuclear form of RNA-editing enzyme ADAR1 promotes ATR activation and resolves genome-wide R-loops, a process that requires its double-stranded RNA-binding domains. Mechanistically, ADAR1 interacts with TOPBP1 and facilitates its loading on perturbed replication forks by enhancing the association of TOPBP1 with RAD9 of the 9-1-1 complex. When replication is inhibited, DNA-RNA hybrid competes with TOPBP1 for ADAR1 binding to promote the translocation of ADAR1 from damaged fork to R-loop region. There, ADAR1 recruits RNA helicases DHX9 and DDX21 to unwind R-loops, simultaneously allowing TOPBP1 to stimulate ATR more efficiently. Collectively, we propose that the tempo-spatially regulated assembly of ADAR1-nucleated protein complexes link R-loop clearance and ATR activation, while R-loops crosstalk with blocked replication forks by transposing ADAR1 to finetune ATR activity and safeguard the genome.