Catálogo de publicaciones - revistas

<jats:title>Making a practical valleytronics device</jats:title> <jats:p> Two-dimensional materials with a hexagonal lattice, such as graphene, have two distinct “valleys” in their band structure. Researchers in the emerging field of valleytronics hope that these valley degrees of freedom can be exploited as information carriers, but making valleytronic devices is tricky. Li <jats:italic>et al.</jats:italic> created chiral valley Hall states on the boundary between oppositely gated regions of bilayer graphene. They then guided these so-called kink states through their sample using spatially modulated gating, demonstrating right and left turns, as well as a valley valve function. </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="6419" page="1149" related-article-type="in-this-issue" vol="362" xlink:href="10.1126/science.aao5989">1149</jats:related-article> </jats:p>

<jats:title>Twisting a route for surface plasmons</jats:title> <jats:p> Graphene is an atomically thin material that supports highly confined plasmon polaritons, or nano-light, with very low loss. The properties of graphene can be made richer by introducing and then rotating a second layer so that there is a slight angle between the atomic registry. Sunku <jats:italic>et al.</jats:italic> show that the moiré patterns that result from such twisted bilayer graphene also provide confined conducting channels that can be used for the directed propagation of surface plasmons. Controlling the structure thereby provides a pathway to control and route surface plasmons for a nanophotonic platform. </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="6419" page="1153" related-article-type="in-this-issue" vol="362" xlink:href="10.1126/science.aau5144">1153</jats:related-article> </jats:p>

<jats:title> Actively persistent <jats:italic>Salmonella</jats:italic> </jats:title> <jats:p> A proportion of <jats:italic>Salmonella</jats:italic> cells can enter a reversible state of growth arrest, which allows them to tolerate environmental stress such as antibiotics. Stapels <jats:italic>et al.</jats:italic> found that these cells are not dormant but are actively modulating their environment. <jats:italic>Salmonella</jats:italic> within their host macrophage niche deployed a specialized type 3 secretory system called SPI-2 to deliver virulence factors, including SteE, into host cells. SteE changed the cytokine profile of the infected macrophages to reprogram them into a noninflammatory and infection-permissive state. Thus, when antibiotics were removed, the <jats:italic>Salmonella</jats:italic> could reemerge and cause disease. </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="6419" page="1156" related-article-type="in-this-issue" vol="362" xlink:href="10.1126/science.aat7148">1156</jats:related-article> </jats:p>

<jats:title>Genetic architecture of developmental disorders</jats:title> <jats:p> The genetics of developmental disorders (DDs) is complex. Martin <jats:italic>et al.</jats:italic> wanted to determine the degree of recessive inheritance of DDs in protein-coding genes. They examined the exomes of more than 6000 families in populations with high and low proportions of consanguineous marriages. They found that 3.6% of DDs in individuals of European ancestry involved recessive coding disorders, less than a tenth of the levels previously estimated. Furthermore, among South Asians with high parental relatedness, rather than most of the disorders arising from inherited variants, fewer than half had a recessive coding diagnosis. </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="6419" page="1161" related-article-type="in-this-issue" vol="362" xlink:href="10.1126/science.aar6731">1161</jats:related-article> </jats:p>

<jats:title>A systematic look at a childhood tumor</jats:title> <jats:p> Neuroblastomas—the most common tumor type in infants—develop from fetal nerve cells, and their clinical course is highly variable. Some neuroblastomas are fatal despite treatment, whereas others respond well to treatment and some undergo spontaneous regression without treatment. Ackermann <jats:italic>et al.</jats:italic> sequenced more than 400 pretreatment neuroblastomas and identified molecular features that characterize the three distinct clinical outcomes. Low-risk tumors lack telomere maintenance mechanisms, intermediate-risk tumors harbor telomere maintenance mechanisms, and high-risk tumors harbor telomere maintenance mechanisms in combination with RAS and/or p53 pathway mutations. </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="6419" page="1165" related-article-type="in-this-issue" vol="362" xlink:href="10.1126/science.aat6768">1165</jats:related-article> </jats:p>

<jats:title>Regulation of RAS by ubiquitination</jats:title> <jats:p> The protein LZTR1 is mutated in human cancers and developmental diseases. Work from two groups now converges to implicate the protein in regulating signaling by the small guanosine triphosphatase RAS. Steklov <jats:italic>et al.</jats:italic> showed that mice haploinsufficient for LZTR1 recapitulated aspects of the human disease Noonan syndrome. Their biochemical studies showed that LZTR1 associated with RAS. LZTR1 appears to function as an adaptor that promotes ubiquitination of RAS, thus inhibiting its signaling functions. Bigenzahn <jats:italic>et al.</jats:italic> found LZTR1 in a screen for proteins whose absence led to resistance to the tyrosine kinase inhibitors used to treat cancers caused by the BCR-ABL oncogene product. Their biochemical studies and genetic studies in fruitflies also showed that loss of LZTR1 led to increased activity of RAS and signaling through the mitogen-activated protein kinase pathway. </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="6419" page="1177" related-article-type="in-this-issue" vol="362" xlink:href="10.1126/science.aap7607">1177</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6419" page="1171" related-article-type="in-this-issue" vol="362" xlink:href="10.1126/science.aap8210">1171</jats:related-article> </jats:p>

<jats:title>Regulation of RAS by ubiquitination</jats:title> <jats:p> The protein LZTR1 is mutated in human cancers and developmental diseases. Work from two groups now converges to implicate the protein in regulating signaling by the small guanosine triphosphatase RAS. Steklov <jats:italic>et al.</jats:italic> showed that mice haploinsufficient for LZTR1 recapitulated aspects of the human disease Noonan syndrome. Their biochemical studies showed that LZTR1 associated with RAS. LZTR1 appears to function as an adaptor that promotes ubiquitination of RAS, thus inhibiting its signaling functions. Bigenzahn <jats:italic>et al.</jats:italic> found LZTR1 in a screen for proteins whose absence led to resistance to the tyrosine kinase inhibitors used to treat cancers caused by the BCR-ABL oncogene product. Their biochemical studies and genetic studies in fruitflies also showed that loss of LZTR1 led to increased activity of RAS and signaling through the mitogen-activated protein kinase pathway. </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="6419" page="1177" related-article-type="in-this-issue" vol="362" xlink:href="10.1126/science.aap7607">1177</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6419" page="1171" related-article-type="in-this-issue" vol="362" xlink:href="10.1126/science.aap8210">1171</jats:related-article> </jats:p>

<jats:title>DNA methylation promotes transcription</jats:title> <jats:p> DNA methylation generally represses transcription, but in some instances, it has also been implicated in transcription activation. Harris <jats:italic>et al.</jats:italic> identified a protein complex in <jats:italic>Arabidopsis</jats:italic> that is recruited to chromatin by DNA methylation. This complex specifically activated the transcription of genes that are already mildly transcribed but had no effect on transcriptionally silent genes such as transposable elements. The complex thereby counteracts the repression effect caused by transposon insertion in neighboring genes while leaving transposons silent. Thus, by balancing both repressive and activating transcriptional effects, DNA methylation can act to fine-tune gene expression. </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="6419" page="1182" related-article-type="in-this-issue" vol="362" xlink:href="10.1126/science.aar7854">1182</jats:related-article> </jats:p>

<jats:title>How membrane viscosity affects respiration</jats:title> <jats:p> In bacteria, energy production by the electron transport chain occurs at cell membranes and can be influenced by the lipid composition of the membrane. Budin <jats:italic>et al.</jats:italic> used genetic engineering to influence the concentration of unsaturated branched-chain fatty acids and thus control membrane viscosity (see the Perspective by Schon). Experimental measurements and mathematical modeling indicated that rates of respiratory metabolism and rates of cell growth were dependent on membrane viscosity and its effects on diffusion. Experiments on yeast mitochondria also showed similar effects. Maintaining efficient respiration may thus place evolutionary constraints on cellular lipid composition. </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="6419" page="1186" related-article-type="in-this-issue" vol="362" xlink:href="10.1126/science.aat7925">1186</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6419" page="1114" related-article-type="in-this-issue" vol="362" xlink:href="10.1126/science.aav7629">1114</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>