Catálogo de publicaciones - revistas

<jats:title>You Snooze, You Lose</jats:title> <jats:p> Sleep serves restorative and memory functions, but it does not always operate analogously across species. Deferral of sleep may be possible when selection strongly favors the awake. <jats:bold> Lesku <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="1654" related-article-type="in-this-issue" vol="337" xlink:href="10.1126/science.1220939">1654</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="1610" related-article-type="in-this-issue" vol="337" xlink:href="10.1126/science.1228466">Siegel</jats:related-article> </jats:bold> ) show that sleep may be deferred without cost or impairment in pectoral sandpipers. These birds breed collectively in the high Arctic, and male competition is intense. Competing for, and displaying to, females are both physically and cognitively demanding, yet birds who slept the least showed no decrease in their ability to perform these activities. Indeed, those males who slept the least obtained the most matings and sired the most offspring. </jats:p>

<jats:title>Limiting Your Options</jats:title> <jats:p> Many species are dependent on specific resources that may limit their range of hosts to that of a few or even a single species. The restriction of the fly <jats:italic>Drosophila pachea</jats:italic> to senita cactus is a classic case of an ecological specialization. <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="1658" related-article-type="in-this-issue" vol="337" xlink:href="10.1126/science.1224829">1658</jats:related-article> ) reveal how multiple amino acid substitutions in the <jats:italic>neverland</jats:italic> gene have rendered <jats:italic>D. pachea</jats:italic> dependent upon the lathosterol of the senita cactus. Thus, relatively few genetic changes can play a large role in determining a species' ecological niche. </jats:p>

<jats:title>Bacterial PERegrinations</jats:title> <jats:p> Many branches of the bacterial domain of life are only known from sequences that turn up in metagenomic analyses and are still only named by acronym—for example, the phylum-level groups BD1-5, OP11, OD1, and the PERs. The parent organisms are probably widespread, but they have not been cultured, and very little is known about their metabolisms or their contributions and functions in the natural environment. <jats:bold> Wrighton <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="1661" related-article-type="in-this-issue" vol="337" xlink:href="10.1126/science.1224041">1661</jats:related-article> ) pumped acetate into an aquifer in Colorado to prompt the naturally occurring bacteria into action and then, from the runoff, filtered out the smaller microbial cells for further analysis. Mass-spectrometry–based proteomics was used to test for functional activity, and 49 distinct genomes were recovered, many with surprising functional attributes. All of the recovered organisms appeared to be strict anaerobes with a full glycolytic pathway that were capable of augmenting energy production by coupling proton-pumping activity to adenosine triphosphate synthase. Several hydrogenases were found that seemed to be able to switch between hydrogen production and polysulfide reduction, depending on the substrate available. Notably, carbon dioxide assimilation was a common feature, with many genes having similarity to those of archaea. </jats:p>

<jats:title>Get Ready, Assemble, Fold</jats:title> <jats:p> The outer membrane protein complex LptD/E is responsible for lipopolysaccharide export to the cell surface of <jats:italic>Escherichia coli.</jats:italic> LptD is an essential β-barrel protein that contains two disulfide bonds between nonconsecutive cysteines. <jats:bold> Chng <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="1665" related-article-type="in-this-issue" vol="337" xlink:href="10.1126/science.1227215">1665</jats:related-article> , published online 30 August) describe the characterization of the oxidative folding and assembly pathway of LptD/E in living cells. A combination of steady-state and pulse-chase measurements was used to identify seven intermediates with different disulfide-bonded states, along the oxidative folding pathway. During folding and assembly, a non-native disulfide-bonded LptD intermediate accumulated and, triggered by β-barrel assembly and association with the lipoprotein LptE, rearranged to the native disulfide-bonded state required for lipopolysaccharide export. Thus, disulfide bond–dependent protein folding can involve the proper assembly of a two-protein complex in order to promote disulfide bond rearrangement. </jats:p>

<jats:title>A Tight Squeeze</jats:title> <jats:p> During intracellular transport, the export of procollagen from the endoplasmic reticulum is intriguing because procollagen is too large to fit into conventional coat protein complex II (COPII)–coated transport vesicles. Recent work has implicated the receptor TANGO1 in procollagen export. Now, <jats:bold> Venditti <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="1668" related-article-type="in-this-issue" vol="337" xlink:href="10.1126/science.1224947">1668</jats:related-article> ) report that TANGO1 recruits Sedlin—also known as TRAPPC2, a homolog of the yeast TRAPP subunit Trs20—and helps to allow COPII-coated carriers to grow large enough to incorporate procollagen. </jats:p>

<jats:title>A Radical Mechanism</jats:title> <jats:p> The bacterial enzyme nitrogenase plays a key role in the global nitrogen cycle by catalyzing the reduction of N <jats:sub>2</jats:sub> to ammonia. At the heart of the enzyme is a metal-sulfur cluster that contains an interstitial light atom recently identified as a carbide. The identification raised questions concerning the role of the carbide in the enzyme mechanism and how it is inserted into the metal cluster. <jats:bold> Wiig <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="1672" related-article-type="in-this-issue" vol="337" xlink:href="10.1126/science.1224603">1672</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="6102" page="1617" related-article-type="in-this-issue" vol="337" xlink:href="10.1126/science.1229088">Boal and Rosenzweig</jats:related-article> </jats:bold> ) now show that the carbide derives from S-adenosylmethionine (SAM) and is inserted into the core by the radical SAM enzyme NifB. </jats:p>

<jats:title>No More Junk DNA</jats:title> <jats:p> The majority of the human genome is transcribed at some level, but the function and evolutionary constraint among regions that do not regulate gene expression or code for genes are generally unknown. Examining data from the 1000 Genomes Project and ENCODE, <jats:bold>Ward and Kellis</jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="1675" related-article-type="in-this-issue" vol="337" xlink:href="10.1126/science.1225057">1675</jats:related-article> , published online 5 September) examined regions of the human genome that did not show conservation among mammals and found evidence for a human lineage-specific constraint spanning approximately 4% of the genome that is biochemically active but not directly associated with genes. Interestingly, these regions showed lower numbers of single-nucleotide polymorphisms, heterozygosity, and derived allele frequencies, suggesting that they are under constraint and may be functional. </jats:p>

<jats:title>Keeping Cancer Cells At Bay</jats:title> <jats:p> Cancer cells are often aneuploid; that is, they have an abnormal number of chromosomes. But to what extent this contributes to the tumorigenic phenotype is not clear. <jats:bold> Senovilla <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="1678" related-article-type="in-this-issue" vol="337" xlink:href="10.1126/science.1224922">1678</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="6102" page="1616" related-article-type="in-this-issue" vol="337" xlink:href="10.1126/science.1228464">Zanetti and Mahadevan</jats:related-article> </jats:bold> ) found that tetraploidization of cancer cells can cause them to become immunogenic and thus aid in their clearance from the body by the immune system. Cells with excess chromosomes put stress on the endoplasmic reticulum, which leads to movement of the protein calreticulin to the cell surface. Calreticulin exposure in turn caused recognition of cancer cells in mice by the host immune system. Thus, the immune system appears to serve a protective role in eliminating hyperploid cells that must be overcome to allow unrestricted growth of cancer cells. </jats:p>

<jats:title>Tuberculosis Vaccine Conundrum</jats:title> <jats:p> Some children experience severe clinical disease when they are vaccinated against tuberculosis, an attenuated live vaccine that is normally innocuous in humans. Several germline mutations have been identified that account for this susceptibility, and now <jats:bold> Bogunovic <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="1684" related-article-type="in-this-issue" vol="337" xlink:href="10.1126/science.1224026">1684</jats:related-article> , published online 2 August) add another to the list— <jats:italic>ISG15</jats:italic> . Uncovering this mutation, which is inherited in an autosomal recessive manner, was a surprise because studies with mice deficient in <jats:italic>ISG15</jats:italic> showed enhanced susceptibility to some viral, but not bacterial, infections. Nevertheless, patients lacking <jats:italic>ISG15</jats:italic> were not able to produce adequate amounts of interferon-γ, a cytokine critical for clearance of the bacteria. </jats:p>

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