Catálogo de publicaciones - revistas

<jats:title>Superconducting Limits</jats:title> <jats:p> An electron wave function extends in three dimensions. Pairing up into Cooper pairs and reducing the temperatures can induce superconductivity in a material. How robust is an inherently three-dimensional effect when the dimensions are restricted? <jats:bold> Qin <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="1314" related-article-type="in-this-issue" vol="324" xlink:href="10.1126/science.1170775">1314</jats:related-article> , published online 30 April) looked at the thickness dependence of superconductivity in thin lead films. In contrast to earlier, less direct measurements, superconductivity was robust, even down to films of only two monolayers. </jats:p>

<jats:title>Defeating the Cuckoo</jats:title> <jats:p> Brood parasite-host interactions show ongoing antagonistic coevolution. What mediates rapid behavioral changes that do not reflect genetic change? <jats:bold>Davies and Welbergen</jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="1318" related-article-type="in-this-issue" vol="324" xlink:href="10.1126/science.1172227">1318</jats:related-article> ) show that reed warblers learn from their neighbors to behave aggressively toward models of the parasitic common cuckoo. Furthermore, reed warblers seem to be predisposed to learn to respond to cuckoos as enemies: Hosts that witnessed neighbors mobbing a harmless parrot model did not increase their aggression toward a cuckoo model. Thus, birds have templates for threats, and relevant antithreat behaviors can be turned on or off depending on social experience. </jats:p>

<jats:title> <jats:italic>Hox</jats:italic> Clocks </jats:title> <jats:p> <jats:italic>Homeobox</jats:italic> or <jats:italic>Hox</jats:italic> genes are historically significant for demonstrating evolutionary conservation and homology in developmentally important genes. In addition, in many species, the <jats:italic>Hox</jats:italic> genes are fundamental to the organization of the embryo. Modifications in the regulation of their colinear, temporal activation may represent a way of altering their expression patterns and to elaborate body plans during evolution. <jats:bold>Soshnikova and Duboule</jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="1320" related-article-type="in-this-issue" vol="324" xlink:href="10.1126/science.1171468">1320</jats:related-article> ) now report highly dynamic modifications of chromatin marks along with progressive <jats:italic>Hox</jats:italic> gene activation during axial extension in the mouse. This work supports the proposal that the “ <jats:italic>Hox</jats:italic> clock” may be controlled, at least in part, by epigenetic mechanisms. </jats:p>

<jats:title>Transcriptional Repressor Dissected</jats:title> <jats:p> Living organisms have quality-control mechanisms to eliminate proteins damaged by environmental stresses. In the model organism <jats:italic>Bacillus subtilis</jats:italic> , the transcriptional repressor CtsR controls the expression of genes that are key to the heat-shock response. CtsR is activated by the kinase McsB to allow transcription of stress response genes, however, the mechanism of activation is unclear. <jats:bold> Fuhrmann <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="1323" related-article-type="in-this-issue" vol="324" xlink:href="10.1126/science.1170088">1323</jats:related-article> ) now describe structural and biochemical studies showing that McsB inhibits DNA binding of CtsR by specifically phosphorylating arginine residues in its DNA binding domain. This study provides a basis for exploring a potential wider role of arginine phosphorylation in prokaryotic and eukaryotic transcriptional regulation. </jats:p>

<jats:title>Rhes-olving Huntington's Disease?</jats:title> <jats:p> Huntington's disease (HD) is caused by a single dominant mutation of huntingtin (Htt), a protein that occurs in all tissues of the body and that is uniformly distributed throughout the brain. How mutant Htt (mHtt) selectively damages striatal neurons with negligible alterations elsewhere has been a mystery. <jats:bold> Subramaniam <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="1327" related-article-type="in-this-issue" vol="324" xlink:href="10.1126/science.1172871">1327</jats:related-article> ) show that Rhes, a small G protein very highly localized to the striatum, binds mHtt and augments its neurotoxicity. Rhes promotes sumoylation of mHtt, leading to its disaggregation and augmented cytotoxicity. The findings establish how mHtt selectively kills cells in the striatum and suggest that Rhes-Htt binding might provide a therapeutic target. </jats:p>

<jats:title>Dissecting VWF's Thrombogenic Potential</jats:title> <jats:p> Von Willebrand factor (VWF) is secreted from cells in an ultralarge form (ULVWF) in response to thrombogenic stimuli. Shear forces expose a binding site for platelets, enabling formation of a hemostatic plug. The thrombogenic potential of VWF correlates with its length and is regulated by proteolytic cleavage of the A2 domain. <jats:bold> Zhang <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="1330" related-article-type="in-this-issue" vol="324" xlink:href="10.1126/science.1170905">1330</jats:related-article> ; see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="1278" related-article-type="in-this-issue" vol="324" xlink:href="10.1126/science.1175874">Gebhardt and Rief</jats:related-article> </jats:bold> ) now combine single molecule data and polymer dynamics theory to show that shear forces in the circulation are sufficient to unfold the A2 domain and allow cleavage of multimers with more than about 200 monomers. The A2 domain may thus represent the “shear bolt” of VWF, unfolding when multimers experience high forces to allow cleavage and down-regulation of thrombogenic potential. </jats:p>

<jats:title>Starving T Cells</jats:title> <jats:p> The T <jats:sub>H</jats:sub> 17 lineage of CD4 <jats:sup>+</jats:sup> helper T cells, characterized by the ability to secrete IL-17, is an important mediator of inflammation and autoimmunity. Dampening the responses of these cells or inhibiting their differentiation is of great therapeutic interest. <jats:bold> Sundrud <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="1334" related-article-type="in-this-issue" vol="324" xlink:href="10.1126/science.1172638">1334</jats:related-article> ; see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="1282" related-article-type="in-this-issue" vol="324" xlink:href="10.1126/science.1175678">Blander and Amsen</jats:related-article> </jats:bold> ) now show that the small molecule halofuginone inhibits the differentiation of T <jats:sub>H</jats:sub> 17 cells but not other CD4 <jats:sup>+</jats:sup> T cell helper lineages both in vitro and in a mouse model of multiple sclerosis. This selective inhibition was mediated by activation of the amino acid starvation response. Amino acid depletion mimicked the effects of halofuginone, whereas excess amino acids rescued T <jats:sub>H</jats:sub> 17 differentiation. The results highlight the importance of amino acid metabolism in regulating inflammation. </jats:p>

<jats:title>Signaling Signature in Situ</jats:title> <jats:p> Upon activation, signaling proteins trigger response pathways, but knowing when and where they are activated within animals has been difficult. <jats:bold>Kamiyama and Chiba</jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="1338" related-article-type="in-this-issue" vol="324" xlink:href="10.1126/science.1170615">1338</jats:related-article> ) describe an in vivo bioprobe imaging technology that reveals the restricted pattern for endogenous activities of a ubiquitously expressed signaling protein Cdc42 within individual cells and in whole animals. Genetic experiments confirmed that it is the activation within individual cells and tissues, not simply the protein's presence, which defines its function during development. </jats:p>

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