Integrative structural analysis of Pseudomonas phage DEV reveals a genome ejection motor.

DEV is an obligatory lytic Pseudomonas phage of the N4-like genus, recently reclassified as Schitoviridae. The DEV genome encodes 91 ORFs, including a 3398 amino acid virion-associated RNA polymerase (vRNAP). Here, we describe the complete architecture of DEV, determined using a combination of cryo-electron microscopy localized reconstruction, biochemical methods, and genetic knockouts.

Search for Rare b→dℓ^{+}ℓ^{-} Transitions at Belle.

We present the results of a search for the b→dℓ^{+}ℓ^{-} flavor-changing neutral-current rare decays B^{+,0}→(η,ω,π^{+,0},ρ^{+,0})e^{+}e^{-} and B^{+,0}→(η,ω,π^{0},ρ^{+})μ^{+}μ^{-} using a 711  fb^{-1} data sample that contains 772×10^{6}  BB[over ¯] events. The data were collected at the ϒ(4S) resonance with the Belle detector at the KEKB asymmetric-energy e^{+}e^{-} collider. We find no evidence for signal and set upper limits on branching fractions at the 90% confidence level in the range (3.

First Measurement of R(X_{τ/ℓ}) as an Inclusive Test of the b→cτν Anomaly.

We measure the tau-to-light-lepton ratio of inclusive B-meson branching fractions R(X_{τ/ℓ})≡B(B→Xτν)/B(B→Xℓν), where ℓ indicates an electron or muon, and thereby test the universality of charged-current weak interactions. We select events that have one fully reconstructed B meson and a charged lepton candidate from 189  fb^{-1} of electron-positron collision data collected with the Belle II detector. We find R(X_{τ/ℓ})=0.

Lack of mTORC2 signaling in CD11c+ myeloid cells inhibits their migration and ameliorates experimental colitis.

The mammalian target of rapamycin (mTOR) pathway plays a key role in determining immune cells function through modulation of their metabolic status. By specific deletion of Rictor in CD11c+ myeloid cells (referred to here as CD11cRicΔ/Δ), we investigated the role of mTOR complex 2 (mTORC2) signaling in dendritic cells (DCs) function in mice. We showed that upon dextran sulfate sodium-induced colitis, the lack of mTORC2 signaling CD11c+ cells diminishes the colitis score and abrogates DC migration to the mesenteric lymph nodes, thereby diminishing the infiltration of T helper 17 cells in the lamina propria and subsequent inflammation.

DUSP3 modulates IRES-dependent translation of mRNAs through dephosphorylation of the HNRNPC protein in cells under genotoxic stimulus.

Background Information: The dual-specificity phosphatase 3 (DUSP3) regulates cell cycle progression, proliferation, senescence, and DNA repair pathways under genotoxic stress. This phosphatase interacts with HNRNPC protein suggesting an involvement in the regulation of HNRNPC-ribonucleoprotein complex stability. In this work, we investigate the impact of DUSP3 depletion on functions of HNRNPC aiming to suggest new roles for this enzyme.