Catálogo de publicaciones - revistas

<jats:title>Sponge Pump</jats:title> <jats:p> “Darwin's Paradox” asks how productive and diverse ecosystems like coral reefs thrive in the marine equivalent of a desert. <jats:bold> De Goeij <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6154" page="108" related-article-type="in-this-issue" vol="342" xlink:href="10.1126/science.1241981">108</jats:related-article> ) now show that coral reef sponges are part of a highly efficient recycling pathway for dissolved organic matter (DOM), converting it, via rapid sponge-cell turnover, into cellular detritus that becomes food for reef consumers. DOM transfer through the sponge loop approaches the gross primary production rates required for the entire coral reef ecosystem. </jats:p>

<jats:title>Silencing a Silent Killer</jats:title> <jats:p> Hypertrophic cardiomyopathy (HCM) is a leading cause of sudden death in young athletes. HCM is caused by dominant mutations in genes encoding constituents of the cardiac sarcomere, the contractile unit that keeps the heart pumping. Studying a mouse model that recapitulates a severe form of HCM caused by a mutation in a β myosin heavy chain gene, <jats:bold> Jiang <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6154" page="111" related-article-type="in-this-issue" vol="342" xlink:href="10.1126/science.1236921">111</jats:related-article> ) investigated whether sarcomere dysfunction could be corrected by selectively silencing expression of the mutant allele. Mice treated shortly after birth with a viral vector encoding an appropriately designed RNA interference cassette did not develop cardiac hypertrophy or myocardial fibrosis—the pathologic manifestations of HCM—for at least 6 months. </jats:p>

<jats:title>pH Gradient in Light of Electroneutrality</jats:title> <jats:p> Photosynthesis in plant chloroplasts depends on a proton gradient to convert light energy into adenosine triphosphate. Studying <jats:italic>Arabidopsis</jats:italic> , <jats:bold> Carraretto <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6154" page="114" related-article-type="in-this-issue" vol="342" xlink:href="10.1126/science.1242113">114</jats:related-article> , published online 5 September; see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6154" page="50" related-article-type="in-this-issue" vol="342" xlink:href="10.1126/science.1244943">Rochaix</jats:related-article> </jats:bold> ) identified the potassium channel TPK3 in the stacked membranes of the chloroplast's thylakoids as key to sustaining the proton gradient. As the thylakoid lumen acidifies on exposure to light, electroneutrality derives from TPK3 activity. TPK3 was able to optimize chloroplast responses to light across a wide range of intensities. Plants lacking functional TPK3 appeared normal when grown at modest light levels, but at higher light levels, the plants showed disruptions in overall growth and in thylakoid organization. </jats:p>

<jats:title>RNA on the Attack</jats:title> <jats:p> Plant microbial pathogens often work through protein effectors that are delivered into the plant cells to disrupt critical cellular functions. <jats:bold> Weiberg <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6154" page="118" related-article-type="in-this-issue" vol="342" xlink:href="10.1126/science.1239705">118</jats:related-article> ; see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6154" page="45" related-article-type="in-this-issue" vol="342" xlink:href="10.1126/science.1245010">Baulcombe</jats:related-article> </jats:bold> ) have now found that small RNAs (sRNAs) of the fungus <jats:italic>Botrytis cinerea</jats:italic> can play a similar role. After fungal infection of tomato or <jats:italic>Arabidopsis</jats:italic> leaves, the plant cells contained a suite of fungal-derived sRNAs. Three sRNAs were found to bind to the plant's own Argonaute protein, thereby silencing the plant's fungal defense genes. </jats:p>

<jats:title>Pumping Out Sodium</jats:title> <jats:p> Mammalian cells contain relatively high concentrations of potassium but low concentrations of sodium. This balance is maintained by an ion pump, the Na <jats:sup>+</jats:sup> , K <jats:sup>+</jats:sup> –adenosine triphosphatase, in an adenosine triphosphate–driven transport cycle that results in the export of three sodium ions and the import of two potassium ions. Structures of potassium-bound conformations of the pump have been determined. Now, <jats:bold> Nyblom <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6154" page="123" related-article-type="in-this-issue" vol="342" xlink:href="10.1126/science.1243352">123</jats:related-article> , published online 19 September) report on the high-resolution crystal structure of a Na <jats:sup>+</jats:sup> -bound conformation, which reveals conformational changes associated with Na <jats:sup>+</jats:sup> binding. </jats:p>

<jats:title>Citation Grabbers</jats:title> <jats:p> Is there quantifiable regularity and predictability in citation patterns? It is clear that papers that have been cited frequently tend to accumulate more citations. It is also clear that, with time, even the most novel paper loses its currency. Some papers, however, seem to have an inherent “fitness” that can be interpreted as a community's response to the research. <jats:bold> Wang <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6154" page="127" related-article-type="in-this-issue" vol="342" xlink:href="10.1126/science.1237825">127</jats:related-article> ; see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6154" page="44" related-article-type="in-this-issue" vol="342" xlink:href="10.1126/science.1245218">Evans</jats:related-article> </jats:bold> ) developed a mechanistic model to predict citation history. The model links a paper's ultimate impact, represented by the total number of citations the paper will ever receive, to a single measurable parameter inferred from its early citation history. The model was used to identify factors that influence a journal's impact factor. </jats:p>

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<jats:p>In an effort to develop more tailored approaches to managing disease, there has been a surge in biomarker research aimed at providing truly personalized medicine. The increase in interest over the past 20 years suggests great promise that biomarkers will transform patient treatment. However, despite the optimism and intense research, relatively few are in routine clinical use today. Attention has now turned to actively translating actionable biomarkers and biomarker signatures into clinical utility—not an easy task. The major reasons for clinical failure of biomarkers are poor experimental design and inappropriate choice of assay. It is therefore critical to carefully construct biomarker discovery and validation studies using the most appropriate assays, and to develop these into validated analytical methods suitable for clinical practice. This webinar will review the unprecedented range of technology choices, and provide insight into the challenges confronting researchers when selecting the right biomarker to pursue and the best assay to develop for the clinic.</jats:p>

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<jats:title>Complexity and Diversity</jats:title> <jats:p> Complex organisms must produce and maintain an extraordinary diversity of cell and tissue types with a limited number of genes and molecular pathways. Cells accomplish this by reusing the same signaling networks at different times, in different tissues, and for different purposes, yet how this context-specificity is achieved is poorly understood. <jats:bold> Jukam <jats:italic>et al.</jats:italic> </jats:bold> ( <jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="uri" xlink:href="http://www.sciencemag.org/content/342/6155/1238016.full">1238016</jats:ext-link> , published online 29 August) show how a set of genes that function in cell and tissue growth can be used again in nondividing fly photoreceptor neurons to ensure that flies develop appropriate sensitivity to both blue and green light. The Hippo pathway undergoes a regulatory change—from negative to positive feedback—that requires a tissue-specific transcription factor network. This network uses evolutionarily conserved regulatory factors whose mutations in humans result in degenerative retinal diseases. The context-appropriate positive feedback in flies ensures an all-or-nothing fate decision necessary to establish a functional visual system. </jats:p>