Dynamics of ultra-intense circularly polarized solitons under inhomogeneous plasmas

The dynamics of the ultra-intense circularly polarized solitons under inhomogeneous plasmas are examined. The interaction is modeled by the Maxwell and relativistic hydrodynamic equations and is solved with fully implicit energy-conserving numerical scheme. It is shown that a propagating weak soliton can be decreased and reflected by increasing plasma background, which is consistent with the existing studies based on hypothesis of weak density response. However it is found that ultra-intense soliton is well trapped and kept still when encountering increasing background. Probably, this founding can be applied for trapping and amplifying high-intensity laser-fields.Comment: 4 pages, 3 figures, submitted to Phys. Plasma

Thermodynamic evidence for pressure-induced bulk superconductivity in the Fe-As pnictide superconductor CaFe2As2

We report specific-heat and resistivity experiments performed in parallel in a Bridgman-type of pressure cell in order to investigate the nature of pressure-induced superconductivity in the iron pnictide compound CaFe2As2. The presence of a pronounced specific-heat anomaly at Tc reveals a bulk nature of the superconducting state. The thermodynamic transition temperature differs dramatically from the onset of the resistive transition. Our data indicates that superconductivity occurs in the vicinity of a crystallographic phase transition. We discuss the discrepancy between the two methods as caused by strain-induced superconducting precursors formed above the bulk thermodynamic transition due to the vicinity of the structural instability

A switch element in the autophagy E2 Atg3 mediates allosteric regulation across the lipidation cascade

Autophagy depends on the E2 enzyme, Atg3, functioning in a conserved E1-E2-E3 trienzyme cascade that catalyzes lipidation of Atg8-family ubiquitin-like proteins (UBLs). Molecular mechanisms underlying Atg8 lipidation remain poorly understood despite association of Atg3, the E1 Atg7, and the composite E3 Atg12-Atg5-Atg16 with pathologies including cancers, infections and neurodegeneration. Here, studying yeast enzymes, we report that an Atg3 element we term E123IR (E1, E2, and E3-interacting region) is an allosteric switch. NMR, biochemical, crystallographic and genetic data collectively indicate that in the absence of the enzymatic cascade, the Atg3(E123IR) makes intramolecular interactions restraining Atg3's catalytic loop, while E1 and E3 enzymes directly remove this brace to conformationally activate Atg3 and elicit Atg8 lipidation in vitro and in vivo. We propose that Atg3's E123IR protects the E2 similar to UBL thioester bond from wayward reactivity toward errant nucleophiles, while Atg8 lipidation cascade enzymes induce E2 active site remodeling through an unprecedented mechanism to drive autophagy

SUMO Modification Stabilizes Enterovirus 71 Polymerase 3D To Facilitate Viral Replication.

Accumulating evidence suggests that viruses hijack cellular proteins to circumvent the host immune system. Ubiquitination and SUMOylation are extensively studied posttranslational modifications (PTMs) that play critical roles in diverse biological processes. Cross talk between ubiquitination and SUMOylation of both host and viral proteins has been reported to result in distinct functional consequences. Enterovirus 71 (EV71), an RNA virus belonging to the family Picornaviridae, is a common cause of hand, foot, and mouth disease. Little is known concerning how host PTM systems interact with enteroviruses. Here, we demonstrate that the 3D protein, an RNA-dependent RNA polymerase (RdRp) of EV71, is modified by small ubiquitin-like modifier 1 (SUMO-1) both during infection and in vitro Residues K159 and L150/D151/L152 were responsible for 3D SUMOylation as determined by bioinformatics prediction combined with site-directed mutagenesis. Also, primer-dependent polymerase assays indicated that mutation of SUMOylation sites impaired 3D polymerase activity and virus replication. Moreover, 3D is ubiquitinated in a SUMO-dependent manner, and SUMOylation is crucial for 3D stability, which may be due to the interplay between the two PTMs. Importantly, increasing the level of SUMO-1 in EV71-infected cells augmented the SUMOylation and ubiquitination levels of 3D, leading to enhanced replication of EV71. These results together suggested that SUMO and ubiquitin cooperatively regulated EV71 infection, either by SUMO-ubiquitin hybrid chains or by ubiquitin conjugating to the exposed lysine residue through SUMOylation. Our study provides new insight into how a virus utilizes cellular pathways to facilitate its replication. IMPORTANCE: Infection with enterovirus 71 (EV71) often causes neurological diseases in children, and EV71 is responsible for the majority of fatalities. Based on a better understanding of interplay between virus and host cell, antiviral drugs against enteroviruses may be developed. As a dynamic cellular process of posttranslational modification, SUMOylation regulates global cellular protein localization, interaction, stability, and enzymatic activity. However, little is known concerning how SUMOylation directly influences virus replication by targeting viral polymerase. Here, we found that EV71 polymerase 3D was SUMOylated during EV71 infection and in vitro Moreover, the SUMOylation sites were determined, and in vitro polymerase assays indicated that mutations at SUMOylation sites could impair polymerase synthesis. Importantly, 3D is ubiquitinated in a SUMOylation-dependent manner that enhances the stability of the viral polymerase. Our findings indicate that the two modifications likely cooperatively enhance virus replication. Our study may offer a new therapeutic strategy against virus replication

Suppressing longitudinal double-layer oscillations by using elliptically polarized laser pulses in the hole-boring radiation pressure acceleration regime

It is shown that well collimated mono-energetic ion beams with a large particle number can be generated in the hole-boring radiation pressure acceleration regime by using an elliptically polarized laser pulse with appropriate theoretically determined laser polarization ratio. Due to the $\bm{J}\times\bm{B}$ effect, the double-layer charge separation region is imbued with hot electrons that prevent ion pileup, thus suppressing the double-layer oscillations. The proposed mechanism is well confirmed by Particle-in-Cell simulations, and after suppressing the longitudinal double-layer oscillations, the ion beams driven by the elliptically polarized lasers own much better energy spectrum than those by circularly polarized lasers.Comment: 6 pages, 5 figures, Phys. Plasmas (2013) accepte