Catálogo de publicaciones - revistas

<jats:title>Slip, Tripped, and Faulted</jats:title> <jats:p> Earthquake risk assessment can be improved if we were able to quantify the recurrence and magnitude of slip events. Until recently though, a lack of sophisticated seismometers has forced us to rely on anecdotal evidence from those who survived major earthquakes or to look for clues in the landscape. <jats:bold> Zielke <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="1119" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1182781">1119</jats:related-article> , published online 21 January; see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="5969" page="1089" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1186770">Scharer</jats:related-article> </jats:bold> ) analyzed high-resolution images of the San Andreas Fault in southern California. The data showed that major surface ruptures, such as the 1857 Fort Tejon earthquake, resulted from slips of only about 5 meters; much less than previously thought. In a study that lends support to this discovery, <jats:bold> Grant Ludwig <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="1117" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1182837">1117</jats:related-article> , published online 21 January; see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="5969" page="1089" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1186770">Scharer</jats:related-article> </jats:bold> ) suggest from analysis of the geomorphic features of this region that several smaller earthquakes have occurred during recent centuries rather than infrequent but larger movements. The Perspective by <jats:bold>Scharer</jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="5969" page="1089" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1186770">1089</jats:related-article> ) discusses how paleoseismological studies like these may be valuable for feeding data into earthquake prediction. </jats:p>

<jats:title>Legume Symbiosome</jats:title> <jats:p> Leguminous plants (peas and beans) are major players in global nitrogen cycling by virtue of their symbioses with nitrogen-fixing bacteria that are harbored in specialized structures, called nodules, on the plant's roots. <jats:bold> Van de Velde <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="1122" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1184057">1122</jats:related-article> ) show that the host plant, <jats:italic>Medicago truncatula</jats:italic> produces nodule-specific cysteine-rich peptides, resembling natural plant defense peptides. The peptides enter the bacterial cells and promote its development into the mature symbiont. In a complementary study, <jats:bold> D. 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" page="1126" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1184096">1126</jats:related-article> ), have identified the signal peptidase, also encoded by the plant, that is required for processing these specialized peptides into their active form. </jats:p>

<jats:title>Legume Symbiosome</jats:title> <jats:p> Leguminous plants (peas and beans) are major players in global nitrogen cycling by virtue of their symbioses with nitrogen-fixing bacteria that are harbored in specialized structures, called nodules, on the plant's roots. <jats:bold> Van de Velde <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="1122" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1184057">1122</jats:related-article> ) show that the host plant, <jats:italic>Medicago truncatula</jats:italic> produces nodule-specific cysteine-rich peptides, resembling natural plant defense peptides. The peptides enter the bacterial cells and promote its development into the mature symbiont. In a complementary study, <jats:bold> D. 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" page="1126" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1184096">1126</jats:related-article> ), have identified the signal peptidase, also encoded by the plant, that is required for processing these specialized peptides into their active form. </jats:p>

<jats:title>Difference, Not Diversity</jats:title> <jats:p> In tropical forests, as in the ocean plankton, thousands of species may compete for the same resources. How they succeed in coexisting remains one of the central paradoxes in the study of biodiversity. Theory shows that coexisting species must partition the environment, but such partitioning is not obvious. Using data from coexisting forest trees in the southeastern United States, <jats:bold>Clark</jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="1129" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1183506">1129</jats:related-article> ) show that individual variation between members of the same species allows them to avoid direct competition: One plant may differ significantly from another in its requirements for light, nutrients, or moisture, yet remain within the general spectrum of features displayed by its conspecifics. </jats:p>

<jats:title>Recombinant Infectious Prions</jats:title> <jats:p> Prion diseases are a group of fatal neurodegenerative disorders that include Creutzfeldt-Jakob disease in humans and bovine spongiform encephalopathy in cows. The prion hypothesis states that the infectious agent of these diseases is an aberrant conformational isoform of the normal prion protein (PrP <jats:sup>C</jats:sup> ), a glycosylphosphatidylinositol-anchored cell surface protein enriched in the central nervous system. The final proof for the prion hypothesis is to convert bacterially expressed recombinant PrP into an infectious prion, but this has been difficult to achieve. <jats:bold> F. 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" page="1132" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1183748">1132</jats:related-article> , published online 28 January; see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="5969" page="1091" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1187790">Supattapone</jats:related-article> </jats:bold> ) put recombinant PrP purified from bacteria into mice and obtained all the characteristics of the infectious agent in prion disease. The recombinant form is not only resistant to proteinase-K, but also shows infectivity in cultured cells and causes rapid disease progression in wild-type mice, yielding both the behavioral and the neuropathological symptoms. </jats:p>

<jats:title>Limiting Inflammatory Signaling</jats:title> <jats:p> Dysregulation of the transcription factor NF-κB causes chronic inflammation, autoimmunity, and malignancy. The zinc-finger protein, A20, is vital for regulating NF-κB signaling, so much so that mice lacking A20 die young of multiorgan failure and cachexia. Similar deficiencies have been seen in Crohn's disease, rheumatoid arthritis, and other inflammatory diseases of humans. But how A20 works has remained unknown. <jats:bold> Shembade <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="1135" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1182364">1135</jats:related-article> ; see the Perspective by <jats:bold> S <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="5969" page="1093" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1187271"> <jats:bold>riskantharajah and Ley</jats:bold> ) </jats:related-article> </jats:bold> have discovered that the A20 protein acts through the ubiquitin labeling system of the cell required for normal protein turnover, and its lack prevents NF-κB recycling, resulting in chronic inflammation. A human T cell lymphotropic virus possesses an oncoprotein that subverts this pathway to the virus' benefit by inhibiting A20 interactions with the ubiquitin pathway to promote NF-κB signaling and cell immortalization. </jats:p>

<jats:title>Tripartite Toxin</jats:title> <jats:p> Luminescent bacterial symbionts of nematode worms that attack insects have long stirred interest in their possibilities for biological control. The bacteria produce a family of toxins composed of at least three subunits that resemble a widely occurring class of bacterial toxins also produced by human pathogens. <jats:bold> Lang <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="1139" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1184557">1139</jats:related-article> ) have elucidated the mode of action and structural interactions of some of these tripartite protein toxins and found that they poison the cell's actin cytoskeleton by catalyzing unusual reactions. One toxin mediated adenosine diphosphate (ADP)–ribosylation at threonine-148 to cause actin polymerization, another ADP-ribosylated Rho protein at glutamine-63, and both synergized to cause actin clustering and cell paralysis. </jats:p>

<jats:title>Bursty, Infrequent Noise</jats:title> <jats:p> In gene regulatory networks, positive feedback loops can give rise to bistability and hysteresis in gene expression, thereby allowing switching mechanisms and memory effects. <jats:bold>To and Maheshri</jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="1142" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1178962">1142</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="5969" page="1088" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1187268">Levens and Gupta</jats:related-article> </jats:bold> ) eschew the commonly held idea that sigmoidal promoter responses are required to achieve a steady-state bimodal response in a positive feedback loop. Instead, using a model and data from an experiment, they favor noisy gene expression and multiple, noncooperative transcription factor binding as an explanation for the bimodal response, and they expect that similar noisy systems are widespread in biology. </jats:p>

<jats:title>Inflexible Timing for Flexibility</jats:title> <jats:p> During critical periods in early life, sensory experience molds circuits in the brain. In the visual cortex, blurring or occluding vision in one eye triggers a rapid reorganization of neuronal responses known as ocular dominance plasticity. The critical period for this plasticity depends on inhibitory neurotransmission. <jats:bold> Southwell <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="1145" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1183962">1145</jats:related-article> ) show that by transplanting embryonic precursors of inhibitory neurons into mice, a period of ocular dominance plasticity can be induced after the end of the normal critical period. These observations suggest that transplantation of inhibitory neurons has therapeutic potential for brain repair and for treating neurological disorders and inducing periods of brain plasticity. </jats:p>

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