Catálogo de publicaciones - revistas

<jats:title>Protein backbone, broken and mended</jats:title> <jats:p> Small, posttranslationally modified peptides are produced by microorganisms as antimicrobial agents or to communicate with neighboring cells. Alterations to the peptide backbone can change the structure of peptides or introduce reactive chemical moieties. Morinaka <jats:italic>et al.</jats:italic> characterized a bacterial enzyme that excises the side chain and α-carbon of a tyrosine residue from a short peptide, leaving behind an α-ketoamide. This backbone functional group is found in some protease inhibitors and is a valuable handle for bio-orthogonal chemistry. The enzyme accepts peptide substrates with a short recognition motif, suggesting that it could be used to generate libraries of modified peptides. </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="6377" page="779" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aao0157">779</jats:related-article> </jats:p>

<jats:title>Forming photonic bound states</jats:title> <jats:p> Photons do not naturally interact with each other and must be coaxed into doing so. Liang <jats:italic>et al.</jats:italic> show that a gas of Rydberg atoms—a cloud of rubidium atoms excited by a sequence of laser pulses—can induce strong interactions between propagating photons. The authors could tune the strength of the interaction to make the photons form dimer and trimer bound states. This approach should prove useful for producing novel quantum states of light and quantum entanglement on demand. </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="6377" page="783" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aao7293">783</jats:related-article> </jats:p>

<jats:title>A way to prevent generalized seizures?</jats:title> <jats:p> Temporal lobe epilepsy is the most common form of epilepsy in adults. Patients have spontaneous seizures and risk developing serious cognitive impairment. Bui <jats:italic>et al.</jats:italic> studied an animal model of temporal lobe epilepsy (see the Perspective by Scharfman). Selective optogenetic inhibition of dentate gyrus mossy cells increased the likelihood of electrographic seizures generalizing to full behavioral convulsive seizures. Activation of mossy cells reduced the likelihood. Thus, the activity of mossy cells might serve to inhibit seizure propagation. </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="6377" page="787" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aan4074">787</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6377" page="740" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aas8993">740</jats:related-article> </jats:p>

<jats:title>Many, many more pollinators needed</jats:title> <jats:p> Numerous studies have shown that biodiversity is necessary for ecosystem function. The majority of these, however, have taken place at relatively small experimental scales. Winfree <jats:italic>et al.</jats:italic> looked across more than 3000 square kilometers for relationships between biodiversity and crop pollination (see the Perspective by Kremen). The number of wild bee species required for successful pollination rapidly increased with spatial scale, largely owing to variation in the species present across sites and the degree to which the most abundant species played a role. In the end, more than an order of magnitude more species than predicted by smaller-scale experiments were required for full ecosystem functioning. </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="6377" page="791" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aao2117">791</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6377" page="741" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aar7614">741</jats:related-article> </jats:p>

<jats:title>Recognizing danger signals</jats:title> <jats:p> In the classical complement pathway, the C1 initiation complex binds to danger patterns on the surface of microbes or damaged host cells and triggers an immune response. Immunoglobulin G (IgG) antibodies form hexamers on cell surfaces that have high avidity for the C1 complex. Ugurlar <jats:italic>et al.</jats:italic> used cryo–electron microscopy to show how a hexamer of C1 complexes interacts with the IgG hexamer. Structure-guided mutagenesis revealed how C1 is activated to trigger an immune response. </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="6377" page="794" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aao4988">794</jats:related-article> </jats:p>

<jats:title>How lipopolysaccharides bridge the gap</jats:title> <jats:p> The outer membrane of Gram-negative bacteria is composed of lipopolysaccharide, a large glycolipid that prevents drugs from entering the cells. Disrupting lipopolysaccharide assembly hypersensitizes bacteria to antibiotics. Sherman <jats:italic>et al.</jats:italic> used biochemical tools to observe lipopolysaccharide transport. Seven proteins, which are conserved in all Gram-negative bacteria, appear to form a protein bridge that uses adenosine triphosphate to power transport of lipopolysaccharide from one membrane to another. The ability to monitor intermembrane transport of lipopolysaccharide will help in efforts to develop and characterize inhibitors. </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="6377" page="798" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aar1886">798</jats:related-article> </jats:p>

<jats:title>SNF'ing out antitumor immunity</jats:title> <jats:p> Immune checkpoint inhibitors induce durable tumor regressions in some, but not all, cancer patients. Understanding the mechanisms that determine tumor sensitivity to these drugs could potentially expand the number of patients who benefit (see the Perspective by Ghorani and Quezada). Pan <jats:italic>et al.</jats:italic> discovered that tumor cells in which a specific SWI/SNF chromatin remodeling complex had been experimentally inactivated were more sensitive to T cell–mediated killing. The cells were more responsive to interferon-γ, leading to increased secretion of cytokines that promote antitumor immunity. Miao <jats:italic>et al.</jats:italic> examined the genomic features of tumors from patients with metastatic renal cell carcinoma who had been treated with immune checkpoint inhibitors. Tumors harboring inactivating mutations in <jats:italic>PBRM1</jats:italic> , which encodes a subunit of the same SWI/SNF complex, were more likely to respond to the drugs. </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="6377" page="770" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aao1710">770</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6377" page="801" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aan5951">801</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6377" page="745" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aat0383">745</jats:related-article> </jats:p>

<jats:p> The 2018 Gordon Research Conference schedule was published on pages 808 to 831 of this issue of the print version of <jats:italic>Science</jats:italic> . The current schedule can also be found online at <jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="uri" xlink:href="http://www.grc.org/">www.grc.org/</jats:ext-link> . </jats:p>

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