Catálogo de publicaciones - revistas

<jats:title>Discovering better theories</jats:title> <jats:p> Theories of human decision-making have proliferated in recent years. However, these theories are often difficult to distinguish from each other and offer limited improvement in accounting for patterns in decision-making over earlier theories. Peterson <jats:italic>et al.</jats:italic> leverage machine learning to evaluate classical decision theories, increase their predictive power, and generate new theories of decision-making (see the Perspective by Bhatia and He). This method has implications for theory generation in other domains. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , abe2629, this issue p. <jats:related-article issue="6547" page="1209" related-article-type="in-this-issue" vol="372">1209</jats:related-article> ; see also abi7668, p. <jats:related-article issue="6547" page="1150" related-article-type="in-this-issue" vol="372">1150</jats:related-article> </jats:p>

<jats:title>How Hedgehog gets its lipid tail</jats:title> <jats:p> Phospholipid membranes serve as barriers between different cellular environments but are also crucial platforms for biosynthesis, signaling, and transport. In animals, the developmental signaling protein Hedgehog must be modified with an acyl group by the membrane-embedded enzyme Hedgehog acyltransferase (HHAT) to be recognized by its receptor. Using cryo–electron microscopy, Jiang <jats:italic>et al.</jats:italic> determined structures of HHAT bound to palmitoyl–coenzyme A or a palmitoylated peptide product. Two cavities connect at the active site, enabling acylation of Hedgehog in the lumen of the endoplasmic reticulum by lipid substrates from the cytosolic face of the membrane. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , abg4998, this issue p. <jats:related-article issue="6547" page="1215" related-article-type="in-this-issue" vol="372">1215</jats:related-article> </jats:p>

<jats:title>Revolution in an RNA-packaging capsid</jats:title> <jats:p> Artificial nucleocapsid proteins, which could be analogous to those used by viruses to package their genomes, are a promising way to protect and deliver RNAs. Using an escalating challenge by nucleases, Tetter <jats:italic>et al.</jats:italic> evolved a protein that forms multimeric, spherical cages into a highly efficient capsid that selectively packages its own encoding RNA. Cryo–electron microscopy of the final design and intermediates revealed a stepwise expansion in size, enabled by destabilizing amino acid substitutions and a domain swap that results in a change of oligomerization interfaces for the base units of the cage. In addition to altering the protein, directed evolution resulted in changes to the encoding RNA structure that enabled efficient uptake versus other cellular RNAs. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , abg2822, this issue p. <jats:related-article issue="6547" page="1220" related-article-type="in-this-issue" vol="372">1220</jats:related-article> </jats:p>

<jats:title>Anti-aging supplement effects in humans</jats:title> <jats:p> Synthesis of nicotinamide adenine dinucleotide (NAD <jats:sup>+</jats:sup> ) decreases during aging, which is thought to limit the activity of enzymes that require it for their catalytic activity. Studies in animals indicate that replenishment of cellular NAD <jats:sup>+</jats:sup> can have beneficial effects on aging and age-related diseases, but the situation in humans is less clear. Yoshino <jats:italic>et al.</jats:italic> report the effects of supplementation with the NAD <jats:sup>+</jats:sup> precursor nicotinamide mononucleotide in overweight or obese postmenopausal women with prediabetes (see the Perspective by Hepler and Bass). The treatment improved insulin sensitivity in muscle, although a change in NAD <jats:sup>+</jats:sup> content was not detected. The treatment also increased the expression of platelet-derived growth factor b. The results support potential therapeutic action of NAD <jats:sup>+</jats:sup> supplementation in humans, but how various NAD+ precursors are processed in specific tissues remains to be fully explored. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , abe9985, this issue p. <jats:related-article issue="6547" page="1224" related-article-type="in-this-issue" vol="372">1224</jats:related-article> ; see also abj0764, p. <jats:related-article issue="6547" page="1147" related-article-type="in-this-issue" vol="372">1147</jats:related-article> </jats:p>

<jats:p> The 2021 Gordon Research Conference schedule was published on pages 1230 to 1233 of this issue of the print version of <jats:italic>Science</jats:italic> . The current schedule can also be found online at <jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="uri" xlink:href="http://www.grc.org/">www.grc.org/</jats:ext-link> . </jats:p>

<jats:title>Stopping the swarm</jats:title> <jats:p> Neutrophils play a major role in the early immune response and are recruited in large numbers into inflamed and infected tissues. By secreting chemoattractants that bind G protein–coupled receptors (GPCRs) on neighboring cells, neutrophils coordinate their behavior as a swarm. Less clear is how this auto-amplifying swarming activity is ultimately turned off. Kienle <jats:italic>et al.</jats:italic> show that desensitization of these GPCRs by the same chemoattractants by GPCR-kinase 2 (GRK2) is one way in which these swarms are shut down (see the Perspective by Rocha-Gregg and Huttenlocher). Unexpectedly, mice with GRK2-deficient neutrophils showed impaired rather than enhanced bacterial clearance. The heightened scanning ability of GRK2-deficient neutrophils may come at the cost of suboptimal phagocytosis and containment of bacteria. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , abe7729, this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" related-article-type="in-this-issue" xlink:href="10.1126/science.abe7729">eabe7729</jats:related-article> ; see also abj3065, p. <jats:related-article issue="6548" page="1262" related-article-type="in-this-issue" vol="372">1262</jats:related-article> </jats:p>

<jats:title>Connecting the dots on white matter</jats:title> <jats:p> The white matter of the brain, which is composed of axonal tracts connecting different brain regions, plays key roles in both normal brain function and a variety of neurological disorders. Zhao <jats:italic>et al.</jats:italic> combined detailed magnetic resonance imaging–based assessment of brain structures with genetic data on nearly 44,000 individuals (see the Perspective by Filley). On the basis of this comprehensive analysis, the authors identified structural and genetic abnormalities associated with neurological and psychiatric disorders, as well as some nondisease traits, thus creating a valuable resource and providing some insights into the underlying neurobiology. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , abf3736, this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" related-article-type="in-this-issue" xlink:href="10.1126/science.abf3736">eabf3736</jats:related-article> ; see also abj1881, p. <jats:related-article issue="6548" page="1265" related-article-type="in-this-issue" vol="372">1265</jats:related-article> </jats:p>

<jats:title>New echolocator</jats:title> <jats:p> Echolocation is a well demonstrated convergent sensory mode in bats and toothed whales. These lineages are not closely related, and this sense might be more broadly distributed than we recognize. Using a suite of approaches, He <jats:italic>et al.</jats:italic> show that the lineage of soft-furred tree mice (genus <jats:italic>Typhlomys</jats:italic> ) includes multiple echolocators. Clear evidence of the behavioral use of echolocation under fully dark conditions was supported by the convergence of ear bone morphology and hearing-related genes with other echolocating mammals. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , aay1513, this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" related-article-type="in-this-issue" xlink:href="10.1126/science.aay1513">eaay1513</jats:related-article> </jats:p>

<jats:p>Climate-forced population displacement is among the greatest human rights issues of our time, presenting unprecedented challenges to communities and the governments responsible for protecting them. Sea level rise, heat, drought, and wildfires will cause people to move, losing homes and places they love, often with no ability to return. Indigenous Peoples have done the least to cause this crisis and face the loss of lands and connections to ancestral, cultural, and spiritual heritage. To ensure that their right to self-determination is protected and the horrific legacy of government-forced relocations is not repeated, communities must lead and define research on climate-forced displacement and managed retreat that involves them and the lands upon which they dwell and subsist. A focus on human rights, and decolonization of research to change institutional structures of knowledge production, can help communities define their future in a climate-altered world.</jats:p>