Catálogo de publicaciones - revistas

<jats:title>Understanding fragile topology</jats:title> <jats:p> Exploiting topological features in materials is being pursued as a route to build in robustness of particular properties. Stemming from crystalline symmetries, such topological protection renders the properties robust against defects and provides a platform of rich physics to be studied. Recent developments have revealed the existence of so-called fragile topological phases, where the means of classification due to symmetry is unclear. Z.-D. Song <jats:italic>et al.</jats:italic> and Peri <jats:italic>et al.</jats:italic> present a combined theoretical and experimental approach to identify, classify, and measure the properties of fragile topological phases. By invoking twisted boundary conditions, they are able to describe the properties of fragile topological states and verify the expected experimental signature in an acoustic crystal. Understanding how fragile topology arises could be used to develop new materials with exotic properties. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6479" page="794" related-article-type="in-this-issue" vol="367" xlink:href="10.1126/science.aaz7650">794</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6479" page="797" related-article-type="in-this-issue" vol="367" xlink:href="10.1126/science.aaz7654">797</jats:related-article> </jats:p>

<jats:title>Redundancy in circadian clocks?</jats:title> <jats:p> The transcription factor BMAL1 is a core component of the mammalian circadian clock; without it, circadian behaviors are abolished. However, Ray <jats:italic>et al.</jats:italic> found that in animals lacking BMAL1, peripheral tissues synchronized with a brief pulse of the glucocorticoid hormone dexamethasone appear to retain a 24-hour pacemaker that sustains rhythmic gene expression, protein abundance, and protein phosphorylation in excised liver cells and fibroblasts (see the Perspective by Brown and Sato). These oscillations persisted in the absence of cues from changes in light or temperature. The results raise intriguing questions about the possible nature of the oscillator that maintains the observed rhythms. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6479" page="800" related-article-type="in-this-issue" vol="367" xlink:href="10.1126/science.aaw7365">800</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6479" page="740" related-article-type="in-this-issue" vol="367" xlink:href="10.1126/science.aba5336">740</jats:related-article> </jats:p>

<jats:title>Strengths and weaknesses of an HIV drug</jats:title> <jats:p> Retroviruses replicate by inserting a copy of their RNA, which has been reverse transcribed into DNA, into the host genome. This process involves the intasome, a nucleoprotein complex comprising copies of the viral integrase bound at the ends of the viral DNA. HIV integrase strand-transfer inhibitors (INSTIs) stop HIV from replicating by blocking the viral integrase and are widely used in HIV treatment. Cook <jats:italic>et al.</jats:italic> describe structures of second-generation inhibitors bound to the simian immunodeficiency virus (SIV) intasome and to an intasome with integrase mutations known to cause drug resistance. Passos <jats:italic>et al.</jats:italic> describe the structures of the HIV intasome bound to a second-generation inhibitor and to developmental compounds that are promising drug leads. These structures show how mutations can cause subtle changes in the active site that affect drug binding, show the basis for the higher activity of later-generation inhibitors, and may guide development of better drugs. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6479" page="806" related-article-type="in-this-issue" vol="367" xlink:href="10.1126/science.aay4919">806</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6479" page="810" related-article-type="in-this-issue" vol="367" xlink:href="10.1126/science.aay8015">810</jats:related-article> </jats:p>

<jats:title>Strengths and weaknesses of an HIV drug</jats:title> <jats:p> Retroviruses replicate by inserting a copy of their RNA, which has been reverse transcribed into DNA, into the host genome. This process involves the intasome, a nucleoprotein complex comprising copies of the viral integrase bound at the ends of the viral DNA. HIV integrase strand-transfer inhibitors (INSTIs) stop HIV from replicating by blocking the viral integrase and are widely used in HIV treatment. Cook <jats:italic>et al.</jats:italic> describe structures of second-generation inhibitors bound to the simian immunodeficiency virus (SIV) intasome and to an intasome with integrase mutations known to cause drug resistance. Passos <jats:italic>et al.</jats:italic> describe the structures of the HIV intasome bound to a second-generation inhibitor and to developmental compounds that are promising drug leads. These structures show how mutations can cause subtle changes in the active site that affect drug binding, show the basis for the higher activity of later-generation inhibitors, and may guide development of better drugs. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6479" page="806" related-article-type="in-this-issue" vol="367" xlink:href="10.1126/science.aay4919">806</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6479" page="810" related-article-type="in-this-issue" vol="367" xlink:href="10.1126/science.aay8015">810</jats:related-article> </jats:p>

<jats:title>Cascading impacts of prey loss</jats:title> <jats:p> The global pandemic caused by the amphibian fungal pathogen <jats:italic>Batrachochytrium dendrobatidis</jats:italic> has decimated frog populations around the world. This decline has been called out as a potential catastrophe for amphibian species. What has been less explored are the impacts of amphibian declines on other members of their ecological communities. Using survey data collected over 13 years, Zipkin <jats:italic>et al.</jats:italic> looked at diversity and body condition of a tropical snake community after amphibians were decimated by chytridiomycosis. They found that the snake community was less diverse and most species were in decline, except for a few “winning” species. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6479" page="814" related-article-type="in-this-issue" vol="367" xlink:href="10.1126/science.aay5733">814</jats:related-article> </jats:p>

<jats:p>A weekly roundup of information on newly offered instrumentation, apparatus, and laboratory materials of potential interest to researchers.</jats:p>