Catálogo de publicaciones - revistas

<jats:title>N on P</jats:title> <jats:p> Nitrogen atoms form strong, relatively unreactive triple bonds with themselves (in N <jats:sub>2</jats:sub> ) and with carbon (in cyanide and nitriles). In contrast, binding to transition metals often leaves an otherwise naked nitrogen center more prone to reactivity. <jats:bold> Dielmann <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="1526" related-article-type="in-this-issue" vol="337" xlink:href="10.1126/science.1226022">1526</jats:related-article> ) prepared a compound with nitrogen bound to divalent phosphorus, which acted more like a metal than a light element. Although the compound, formally a nitrene, was sufficiently stable to isolate at room temperature and characterize by x-ray diffraction, it transferred the nitrogen efficiently to unsaturated carbon compounds. </jats:p>

<jats:title>Minimal Ice</jats:title> <jats:p> Water clusters comprising fewer than 100 molecules have long been studied in gas phase to model the more complex structures of ice and liquid water. At some stage, as clusters grow larger, they effectively become tiny crystals of ice, but it has been hard to pinpoint precisely where in the range between 100 and 1000 molecules the formal transition takes place. <jats:bold> Pradzynski <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="1529" related-article-type="in-this-issue" vol="337" xlink:href="10.1126/science.1225468">1529</jats:related-article> ) used vibrational spectroscopy to show that the onset of an icelike structure, indicated by a characteristically distinct absorption band in the infrared, occurs at a cluster size of approximately 275 molecules. </jats:p>

<jats:title>Motoring Along</jats:title> <jats:p> Dyneins are large and complex molecular motors that transport cargo along cellular microtubules and power the movement of cilia. An enigma is how microtubule binding and nucleotide hydrolysis are coordinated between sites separated by 25 nm. <jats:bold> Redwine <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="1532" related-article-type="in-this-issue" vol="337" xlink:href="10.1126/science.1224151">1532</jats:related-article> ) report an electron microscopy structure of the dynein microtubule-binding domain bound to microtubules in a high-affinity state and combined this with molecular dynamics and existing x-ray structures to provide a model for how dynein couples its affinity for microtubules with the nucleotide-bound state of the motor domain. </jats:p>

<jats:title>What Kitty Shares with Kings</jats:title> <jats:p> Although long-studied, the underlying basis of mammalian coat patterns remains unclear. By studying a large number of cat species and varieties, <jats:bold> Kaelin <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="1536" related-article-type="in-this-issue" vol="337" xlink:href="10.1126/science.1220893">1536</jats:related-article> ) identified two genes, <jats:italic>Taqpep</jats:italic> and <jats:italic>Edn3</jats:italic> , as critical factors in the development of feline pigment patterns. Mutations in <jats:italic>Taqpep</jats:italic> are responsible for the blotched tabby pattern in domestic cats and the unusual coat of wild king cheetahs. Gene expression patterns in cat and cheetah skin suggest that <jats:italic>Edn3</jats:italic> is a likely regulator of felid hair color. The findings support a common model for coat and pigment pattern formation in domestic and wild cats. </jats:p>

<jats:title>Identifying BAP1 Targets</jats:title> <jats:p> Inactivating mutations in the deubiquitinating enzyme BAP1 have been associated with cancer. <jats:bold> Dey <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="1541" related-article-type="in-this-issue" vol="337" xlink:href="10.1126/science.1221711">1541</jats:related-article> , published online 9 August; see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6101" page="1463" related-article-type="in-this-issue" vol="337" xlink:href="10.1126/science.1228463">White and Harper</jats:related-article> </jats:bold> ) reveal molecular targets of the enzyme and show evidence for a role in leukemia. Mice specifically lacking the target of BAP1, HCF-1, in the bone marrow developed myeloid leukemia. BAP1 appears to be part of a complex that regulates modification of histones and gene expression important for normal hematopoiesis and tumor suppression. </jats:p>

<jats:title>Fixing on a Marine Partnership</jats:title> <jats:p> Nitrogen fixation by microorganisms determines the productivity of the biosphere. Although plants photosynthesize by virtue of the ancient incorporation of cyanobacteria to form chloroplasts, no equivalent endosymbiotic event has occurred for nitrogen fixation. Nevertheless, in terrestrial environments, nitrogen-fixing symbioses between bacteria and plants, for example, are common. <jats:bold> Thompson <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="1546" related-article-type="in-this-issue" vol="337" xlink:href="10.1126/science.1222700">1546</jats:related-article> ) noticed that the ubiquitous marine cyanobacterium UCYN-A has an unusually streamlined genome lacking components of the photosynthetic machinery and central carbon metabolism—all suggestive of being an obligate symbiont. By using gentle filtration methods for raw seawater, a tiny eukaryote partner for UCYN-A of less than 3-µm in diameter was discovered. The bacterium sits on the cell wall of this calcifying picoeukaryote, donating fixed nitrogen and receiving fixed carbon in return. </jats:p>

<jats:title>Removing Fear Memories</jats:title> <jats:p> Disruption of reconsolidation of an activated fear memory prevents subsequent fear expression. After a memory reminder, extinction training can disrupt fear memory. In rodents, this process is dependent on a brain area called the amygdala. <jats:bold> Agren <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="1550" related-article-type="in-this-issue" vol="337" xlink:href="10.1126/science.1223006">1550</jats:related-article> ) used functional magnetic resonance imaging and a fear conditioning paradigm to show in humans that, after an associative fear memory was formed, reactivation and reconsolidation left a signature in the basolateral amygdala. This memory trace predicted later fear expression, which was linked to activity in areas forming the fear circuit of the brain. Extinction alone did not change this signal. However, extinction in the reconsolidation window blocked fear expression by erasing the fear memory trace in the amygdala and weakened the connection in the wider fear circuit of the brain. </jats:p>

<jats:title>Recognizing Escaped Commensals</jats:title> <jats:p> In order to coexist peacefully, the billions of bacteria in our gut and our immune system have reached a détente. An intestinal mucosal firewall exists, so bacteria remain localized to the gut, where the immune system is tightly regulated so that these bacteria are tolerated. Enteric infections, however, lead to a breach in this mucosal firewall, resulting in exposure of the peripheral immune system to the intestinal bacterial contents. What is the result? Using oral <jats:italic>Toxoplasma gondii</jats:italic> infection in mice, <jats:bold> Hand <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="1553" related-article-type="in-this-issue" vol="337" xlink:href="10.1126/science.1220961">1553</jats:related-article> , published online 23 August) show that, besides the <jats:italic>T. gondii</jats:italic> –specific T cell response, a commensal bacteria–specific T cell response is elicited. The CD4 <jats:sup>+</jats:sup> T cell–specific response was tracked to a commensal-derived flagellin, and these T cells expanded after <jats:italic>T. gondii</jats:italic> infection and formed long-lived memory cells able to respond to subsequent challenges. Thus, enteric infections can lead to the formation of commensal bacteria–specific, long-lived memory T cells that reside throughout the body—which may play a role in intestinal pathologies such as inflammatory bowel disease. </jats:p>

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