Catálogo de publicaciones - revistas

<jats:title>The peopling of Tibet</jats:title> <jats:p> The date of the first permanent human occupation of the high Tibetan Plateau has been estimated at about 3600 years ago, when agriculture became established. Meyer <jats:italic>et al.</jats:italic> used several dating techniques to analyze sediments at a high-altitude site (4270 m) where human handprints and footprints have been found. Their analysis indicates occupation of the plateau 7400 years ago and possibly earlier. These dates are consistent with the genetic history of Tibetans and suggest that a permanent preagricultural peopling of the plateau was enabled by the wetter regional climate at that time. </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="6320" page="64" related-article-type="in-this-issue" vol="355" xlink:href="10.1126/science.aag0357">64</jats:related-article> </jats:p>

<jats:title>Brain structure and function mature together</jats:title> <jats:p> Our ability to recognize faces improves from infancy to adulthood. This improvement depends on specific face-selective regions in the visual system. Gomez <jats:italic>et al.</jats:italic> tested face memory and place recognition in children and adults while scanning relevant brain regions. Anatomical changes co-occurred with functional changes in the brain. Some regions in the high-level visual cortex showed profound developmental maturation, whereas others were stable. Thus, improvements in face recognition involve an interplay between structural and functional changes in the brain. </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="6320" page="68" related-article-type="in-this-issue" vol="355" xlink:href="10.1126/science.aag0311">68</jats:related-article> </jats:p>

<jats:title>Shedding light on fossil lantern fruit</jats:title> <jats:p> The Solanaceae (or nightshades) are one of the best-studied plant families, yet their evolutionary origins have thus far been relatively obscure. Corroborative fossil evidence of molecular phylogenetic divergence dates has been lacking. Wilf <jats:italic>et al.</jats:italic> present 52-million-year-old fossils of lantern fruits from Argentina, which they ascribe to the modern genus <jats:italic>Physalis.</jats:italic> These fossil finds suggest a much earlier origin of the lantern fruit lineage and indicate that the Solanaceae may have diversified before the final breakup of the Gondwanan supercontinent. </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="6320" page="71" related-article-type="in-this-issue" vol="355" xlink:href="10.1126/science.aag2737">71</jats:related-article> </jats:p>

<jats:title>Sweet, but not too sweet</jats:title> <jats:p> Nectar-feeding pollinators, when given a choice, tend to prefer nectar with high concentrations of sugar. Nectar-producing plants, however, tend to produce more dilute nectar. This mismatch between selective force and trait value has long been seen as an evolutionary paradox. Nachev <jats:italic>et al.</jats:italic> used a dynamic flower array that evolved in real time in a Costa Rican rainforest to show that the “paradox” is, in fact, driven by pollinator choices (see the Perspective by Farris). Bat pollinators based their choices on small, nonlinear differences in nectar sweetness, which led to selection for less sweet nectar overall. </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="6320" page="75" related-article-type="in-this-issue" vol="355" xlink:href="10.1126/science.aah4219">75</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6320" page="25" related-article-type="in-this-issue" vol="355" xlink:href="10.1126/science.aal4193">25</jats:related-article> </jats:p>

<jats:title>Evading cancer drugs by identity fraud</jats:title> <jats:p> Prostate cancer growth is fueled by male hormones called androgens. Drugs targeting the androgen receptor (AR) are initially efficacious, but most tumors eventually become resistant (see the Perspective by Kelly and Balk). Mu <jats:italic>et al.</jats:italic> found that prostate cancer cells escaped the effects of androgen deprivation therapy through a change in lineage identity. Functional loss of the tumor suppressors TP53 and RB1 promoted a shift from AR-dependent luminal epithelial cells to AR-independent basal-like cells. In related work, Ku <jats:italic>et al.</jats:italic> found that prostate cancer metastasis, lineage switching, and drug resistance were driven by the combined loss of the same tumor suppressors and were accompanied by increased expression of the epigenetic regulator Ezh2. Ezh2 inhibitors reversed the lineage switch and restored sensitivity to androgen deprivation therapy in experimental models. </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="6320" page="84" related-article-type="in-this-issue" vol="355" xlink:href="10.1126/science.aah4307">84</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6320" page="78" related-article-type="in-this-issue" vol="355" xlink:href="10.1126/science.aah4199">78</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6320" page="29" related-article-type="in-this-issue" vol="355" xlink:href="10.1126/science.aam5355">29</jats:related-article> </jats:p>

<jats:title>Evading cancer drugs by identity fraud</jats:title> <jats:p> Prostate cancer growth is fueled by male hormones called androgens. Drugs targeting the androgen receptor (AR) are initially efficacious, but most tumors eventually become resistant (see the Perspective by Kelly and Balk). Mu <jats:italic>et al.</jats:italic> found that prostate cancer cells escaped the effects of androgen deprivation therapy through a change in lineage identity. Functional loss of the tumor suppressors TP53 and RB1 promoted a shift from AR-dependent luminal epithelial cells to AR-independent basal-like cells. In related work, Ku <jats:italic>et al.</jats:italic> found that prostate cancer metastasis, lineage switching, and drug resistance were driven by the combined loss of the same tumor suppressors and were accompanied by increased expression of the epigenetic regulator Ezh2. Ezh2 inhibitors reversed the lineage switch and restored sensitivity to androgen deprivation therapy in experimental models. </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="6320" page="84" related-article-type="in-this-issue" vol="355" xlink:href="10.1126/science.aah4307">84</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6320" page="78" related-article-type="in-this-issue" vol="355" xlink:href="10.1126/science.aah4199">78</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6320" page="29" related-article-type="in-this-issue" vol="355" xlink:href="10.1126/science.aam5355">29</jats:related-article> </jats:p>

<jats:title>High-resolution insights into the intasome</jats:title> <jats:p> An essential step in the life cycle of lentiviruses such as HIV-1 is when viral DNA integrates into the host genome, establishing a permanent infection of the host cell. The viral integrase enzyme catalyzes this process and is a major drug target. During viral integration, integrase binds the ends of viral DNA, forming a higher-order structure called the intasome. Passos <jats:italic>et al.</jats:italic> and Ballandras-Colas <jats:italic>et al.</jats:italic> used cryo—electron microscopy to solve the structures of the intasomes from HIV-1 and maedi-visna virus (ovine lentivirus), respectively. These structures reveal how integrase self-associates to form a functional intasome and help resolve previous conflicting models of intasome assembly. </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="6320" page="89" related-article-type="in-this-issue" vol="355" xlink:href="10.1126/science.aah5163">89</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6320" page="93" related-article-type="in-this-issue" vol="355" xlink:href="10.1126/science.aah7002">93</jats:related-article> </jats:p>

<jats:title>High-resolution insights into the intasome</jats:title> <jats:p> An essential step in the life cycle of lentiviruses such as HIV-1 is when viral DNA integrates into the host genome, establishing a permanent infection of the host cell. The viral integrase enzyme catalyzes this process and is a major drug target. During viral integration, integrase binds the ends of viral DNA, forming a higher-order structure called the intasome. Passos <jats:italic>et al.</jats:italic> and Ballandras-Colas <jats:italic>et al.</jats:italic> used cryo—electron microscopy to solve the structures of the intasomes from HIV-1 and maedi-visna virus (ovine lentivirus), respectively. These structures reveal how integrase self-associates to form a functional intasome and help resolve previous conflicting models of intasome assembly. </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="6320" page="89" related-article-type="in-this-issue" vol="355" xlink:href="10.1126/science.aah5163">89</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6320" page="93" related-article-type="in-this-issue" vol="355" xlink:href="10.1126/science.aah7002">93</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>