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<jats:title>A gentle reconstruction</jats:title> <jats:p> Changes in the volume of a material’s Fermi surface are typically associated with the breaking of symmetry. Maksimovic <jats:italic>et al</jats:italic> . found evidence for an unusual type of this Fermi surface reconstruction, one without symmetry breaking, in the heavy fermion compound cerium cobalt indium (CeCoIn <jats:sub>5</jats:sub> ). Doping the material with tin led to abrupt changes in Hall effect, quantum oscillation, and photoemission signals. The researchers interpret the findings in terms of the delocalization of f-electrons associated with cerium atoms. —JS </jats:p>

<jats:title>Dendritic spines’ electrical function?</jats:title> <jats:p> Dendritic spines are small protrusions that cover the dendrites of most neurons in the brain. Their electrical properties are still controversially discussed. Cornejo <jats:italic>et al</jats:italic> . used an array of techniques to investigate the degree of voltage attenuation by dendritic spine necks in pyramidal neurons of the mouse neocortex. Spines not only synchronously depolarized in response to backpropagating action potentials, but local and transient depolarization also occurred. Isolated depolarization in individual spines reflected localized synaptic activation. A significant voltage gradient between dendritic spine and dendrite indicated that spines may constitute elementary electric compartments. The spine neck resistance is thus not negligible and may substantially contribute to the regulation of synaptic efficacy in the central nervous system. —PRS </jats:p>

<jats:title>Not your typical GPCR</jats:title> <jats:p> Among the large family of G protein–coupled receptors (GPCRs) are many orphans, so called because their signaling reactions remain poorly understood. Among these is GPR158 which is highly expressed in the nervous system and implicated in processes from cognition to memory to mood. Patil <jats:italic>et al</jats:italic> . determined a high-resolution structure of GPR158 alone and bound to a regulator of G protein signaling (RGS) complex. GPR158 has an unusual dimerization mode with an extensive interaction interface that locks it in a conformation that likely prevents G protein activation. RGS binds to the homodimer at a site that substantially overlaps the surface that binds G proteins, again preventing canonical G protein signaling. Binding of a ligand to the extracellular domain may regulate signaling through the RGS complex. —VV </jats:p>

<jats:title>Making CAR T cells in vivo</jats:title> <jats:p> Cardiac fibrosis is the stiffening and scarring of heart tissue and can be fatal. Rurik <jats:italic>et al</jats:italic> . designed an immunotherapy strategy to generate transient chimeric antigen receptor (CAR) T cells that can recognize the fibrotic cells in the heart (see the Perspective by Gao and Chen). By injecting CD5-targeted lipid nanoparticles containing the messenger RNA (mRNA) instructions needed to reprogram T lymphocytes, the researchers were able to generate therapeutic CAR T cells entirely inside the body. Analysis of a mouse model of heart disease revealed that the approach was successful in reducing fibrosis and restoring cardiac function. The ability to produce CAR T cells in vivo using modified mRNA may have a number of therapeutic applications. —PNK </jats:p>

<jats:title>Consuming oxygen, but making it too</jats:title> <jats:p> For marine microbes, there are myriad biological reactions involved in the cycling of nutrients and the generation of energy. Availability of oxygen is crucial for many species’ metabolism. Kraft <jats:italic>et al</jats:italic> . were surprised to find that pure cultures of an ammonia-oxidizing archaean (AOA) (see the Perspective by Martens-Habbena and Qin), <jats:italic>Nitosopumilus maritimus</jats:italic> , were able to regenerate small amounts of oxygen when placed under anoxic conditions. Isotope labeling of nitrogen species revealed a series of reactions transforming nitrite, the expected metabolic end product, into nitric oxide, nitrous oxide, and, eventually, dinitrogen. Oxygen was also formed, likely from nitric oxide disproportionation, but was mostly consumed, which is consistent with the overall aerobic metabolism of AOA. These organisms can be found in oxygen-depleted waters and may benefit from producing oxygen from nitrite under these conditions. —MAF </jats:p>

<jats:title>Species shifts</jats:title> <jats:p> Our anthropogenically warmed climate will lead to a suite of organismal changes. To predict how some of these may occur, we can look to past warm (interglacial) periods. Salvatteci <jats:italic>et al</jats:italic> . used this approach and looked at a marine sediment record of the Humboldt Current system off the coast of Peru (see the Perspective by Yasuhara and Deutsch). They found that previous warm periods were dominated by small, goby-like fishes, whereas this ecosystem currently is dominated by anchovy-like fishes. Such a shift is not only relevant to ecosystem shifts but also to fisheries because anchovies are heavily fished as a food source and gobies are much less palatable than anchovies. —SNV </jats:p>

<jats:title>A block to viral cell entry</jats:title> <jats:p> Crimean-Congo hemorrhagic fever virus is a tickborne virus that can cause severe disease and even death in humans. Disease occurrence is linked to the geographic range of the tick vector, and climate change may increase this range. Infection of host cells requires the fusion glycoprotein Gc, which is the main target of neutralizing antibodies. Mishra <jats:italic>et al</jats:italic> . build on previous work that identified a combination of two Gc-targeting antibodies that gave postexposure protection in an animal model. The authors determined the structure of the antigen-binding fragments of the two antibodies bound to a prefusion form of Gc and also the structure of Gc after the conformational change into the trimeric postfusion form. The structures show how the antibodies work together to block membrane fusion. —VV </jats:p>

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<jats:title>Mitochondria shed their SPOTs</jats:title> <jats:p> Outer mitochondrial membrane (OMM) function is essential for cellular health. How mitochondria respond to naturally occurring OMM stress is unknown. Li <jats:italic>et al</jats:italic> . show that, upon infection with the human parasite <jats:italic>Toxoplasma gondii</jats:italic> , mitochondria shed large structures positive for OMM (SPOTs). SPOT formation required the parasite effector TgMAF1 and its interaction with the host mitochondrial receptor TOM70 and translocase SAM50. TOM70-dependent SPOT formation mediated a depletion of mitochondrial proteins and optimal parasite growth. SPOT-like structures also formed after OMM perturbations independently of infection. Thus, membrane remodeling is a feature of cellular responses to OMM stress that <jats:italic>Toxoplasma</jats:italic> hijacks during infection. —SMH </jats:p>