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Shirogane, Y.

Publications and source records attributed to Shirogane, Y..

3 recordsLinked to original sources

Glycolipid MPIase is essential for the TAT (Twin-Arginine Translocation) pathway

TAT (Twin-Arginine Translocation) is a preprotein translocation system dedicated to membrane translocation of prefolded proteins in plants and bacteria. The TAT translocon, consisting of the TatABC subunits, drives translocation using proton motive force. However, there have been no reports on the successful reconstitution of the TAT system. In this report, we show that MPIase, a glycolipid that has been known to catalyze membrane protein integration, is essential for the TAT system. Our findings in recombinant Escherichia coli demonstrate that overproducing TatABC increases MPIase levels and that depleting MPIase results in TAT precursor accumulation in the cytosol. Furthermore, co-reconstitution of MPIase with TatABC revealed the translocation activities of TAT substrates in a proton motive force-dependent manner. This is the first successful reconstitution of the TAT system and will be advantageous for understanding its mechanisms.

biochemistry↗

Experimental and mathematical insights on the interactions between poliovirus and a defective interfering genome

1During replication, RNA viruses accumulate genome alterations, such as mutations and deletions. The interactions between individual variants can determine the fitness of the virus population and, thus, the outcome of infection. To investigate the effects of defective interfering genomes (DI) on wild-type (WT) poliovirus replication, we developed an ordinary differential equation model. We experimentally determined virus and DI replication during co-infection, and use these data to infer model parameters. Our model predicts, and our experimental measurements confirm, that DI replication and encapsidation are the most important determinants for the outcome of the competition. WT replication inversely correlates with DI replication. Our model predicts that genome replication and effective DI genome encapsidation are critical to effectively inhibit WT production, but an equilibrium can be established which enables WT to replicate, albeit to reduce levels.

microbiology↗

Experimental and mathematical insights on the competition between poliovirus and a defective interfering genome

During replication, RNA virus populations accumulate genome alterations, such as mutations and deletions. The interactions between individual variants within the population can determine the fitness of the virus and, thus, the outcome of infection. We developed an ordinary differential equation model to infer the effect of the interaction between defective interfering (DI) replicons and wild-type (WT) poliovirus. We measure production of RNA and viral particles during a single infection cycle, and use these data to infer model parameters. We find that DI replicates faster than WT, but an equilibrium is established when both WT and DI compete for resources needed for RNA replication and genome encapsidation. In the presence of DI, the concentration of WT virions at cell lysis is suppressed by the factor of 5. Multiple generations within a single cell infection provide opportunities for significant inhibition of WT replication by competition with the faster replicating DI genomes.

microbiology↗