Translation of most mRNAs is suppressed under stress conditions. Phosphorylation of the a-subunit of eukaryotic translation initiation factor 2 (eIF2), which delivers initiator tRNA (Met-tRNA i ) to the P site of the 40S ribosomal subunit, is responsible for such translational suppression. However, translation of hepatitis C viral (HCV) mRNA is refractory to the inhibitory effects of eIF2a phosphorylation, which prevents translation by disrupting formation of the eIF2-GTP-Met-tRNA i ternary complex. Here, we report that eIF2A, an alternative initiator tRNA-binding protein, has a key role in the translation of HCV mRNA during HCV infection, in turn promoting eIF2a phosphorylation by activating the eIF2a kinase PKR. Direct interaction of eIF2A with the IIId domain of the HCV internal ribosome entry site (IRES) is required for eIF2A-dependent translation. These data indicate that stress-independent translation of HCV mRNA occurs by recruitment of eIF2A to the HCV IRES via direct interaction with the IIId domain and subsequent loading of Met-tRNA i to the P site of the 40S ribosomal subunit.

We report on the experimental observation of vortex cluster shedding from a moving obstacle in an oblate atomic Bose-Einstein condensate. At low obstacle velocities v above a critical value, vortex clusters consisting of two like-sign vortices are generated to form a regular configuration like a von Kármán street, and as v is increased, the shedding pattern becomes irregular with many different kinds of vortex clusters. In particular, we observe that the Stouhal number associated with the shedding frequency exhibits saturation behavior with increasing v. The regular-to-turbulent transition of the vortex cluster shedding reveals remarkable similarities between a superfluid and a classical viscous fluid. Our work opens a new direction for experimental investigations of the superfluid Reynolds number characterizing universal superfluid hydrodynamics.

The signaling lipid molecule 15-deoxy-delta 12,14-prostaglandin J2 (15d-PGJ2) has multiple cellular functions, including anti-inflammatory and antineoplastic activities. Here, we report that 15d-PGJ2 blocks translation through inactivation of translational initiation factor eIF4A. Binding of 15d-PGJ2 to eIF4A blocks the interaction between eIF4A and eIF4G that is essential for translation of many mRNAs. Cysteine 264 in eIF4A is the target site of 15d-PGJ2. The antineoplastic activity of 15d-PGJ2 is likely attributed to inhibition of translation. Moreover, inhibition of translation by 15d-PGJ2 results in stress granule (SG) formation, into which TRAF2 is sequestered. The sequestration of TRAF2 contributes to the anti-inflammatory activity of 15d-PGJ2. These findings reveal a novel crosstalk between translation and inflammatory response, and offer new approaches to develop anticancer and antiinflammatory drugs that target translation factors including eIF4A.

In a two-dimensional (2D) classical fluid, a large-scale flow structure emerges out of turbulence, which is known as the inverse energy cascade where energy flows from small to large length scales. An interesting question is whether this phenomenon can occur in a superfluid, which is inviscid and irrotational by nature. Atomic Bose-Einstein condensates (BECs) of highly oblate geometry provide an experimental venue for studying 2D superfluid turbulence, but their full investigation has been hindered due to a lack of the circulation sign information of individual quantum vortices in a turbulent sample. Here, we demonstrate a vortex sign detection method by using Bragg scattering, and we investigate decaying turbulence in a highly oblate BEC at low temperatures, with our lowest being ~0.5T c, where T c is the superfluid critical temperature. We observe that weak spatial pairing between vortices and antivortices develops in the turbulent BEC, which corresponds to the vortex-dipole gas regime predicted for high dissipation. Our results provide a direct quantitative marker for the survey of various 2D turbulence regimes in the BEC system.