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<jats:title>More Than the Sum of the Parts</jats:title> <jats:p> The radiative output of the Sun varies distinctly with the 11-year cycle of sunspots, although the change in energy output is small—less than a tenth of a percent in magnitude. Nevertheless, that small variation produces changes in sea surface temperatures two or three times as large as it should, and the mechanism by which this occurs has remained unclear. <jats:bold> Meehl <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="1114" related-article-type="in-this-issue" vol="325" xlink:href="10.1126/science.1172872">1114</jats:related-article> ; see the news story by <jats:bold> <jats:related-article issue="5944" page="1058-b" related-article-type="in-this-issue" vol="325">Kerr</jats:related-article> </jats:bold> ) employ three global, coupled climate models to simulate this phenomenon. Two mechanisms appear to act in conjunction to cause this ocean response: a change in the abundance of stratospheric ozone owing to fluctuations of shortwave solar forcing; and a coupled surface ocean-atmosphere response. This combination of effects enhances precipitation maxima, reduces low-latitude cloud cover, and lowers the temperature of surface waters in the tropical Pacific Ocean, resulting in the larger warm-to-cold variation. </jats:p>

<jats:title>“Rapid” Recovery</jats:title> <jats:p> The Permian-Triassic extinction 252 million years ago was Earth's most severe biotic crisis since the Precambrian and is thought to have depressed diversity in its wake for millions of years. <jats:bold> Brayard <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="1118" related-article-type="in-this-issue" vol="325" xlink:href="10.1126/science.1174638">1118</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="5944" page="1079" related-article-type="in-this-issue" vol="325" xlink:href="10.1126/science.1178325">Marshall and Jacobs</jats:related-article> </jats:bold> ) show, however, that ammonoids, a large group of marine organisms that were severely affected, recovered remarkably quickly. Only 1 million years after the extinction, ammonoids had recovered to levels higher than in the Permian, compared with the 10-million-year biotic recovery period for other benthic organisms. The Triassic recovery seems to include several cycles, but the immediate recovery of ammonoids may have left them as one of the most diverse groups in the earliest Triassic. </jats:p>

<jats:title>Assessing Ecological Restoration</jats:title> <jats:p> In the wake of the Millennium Ecosystem Assessment, the analysis of ecosystem services, and their relationship to biodiversity, has become one of the most rapidly developing research themes in environmental science. At the same time, ecological restoration is widely being implemented as a response to environmental degradation and biodiversity loss. <jats:bold> Rey Benayas <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="1121" related-article-type="in-this-issue" vol="325" xlink:href="10.1126/science.1172460">1121</jats:related-article> , published online 30 July) link these themes in a meta-analysis of the impacts of ecological restoration actions on provision of ecosystem services and biodiversity conservation. The analysis of 89 published restoration projects worldwide establishes that ecological restoration does, in general, have positive impacts on both biodiversity and provision of ecosystem services. These effects are especially marked in the tropics. Thus, ecological restoration actions may indeed deliver benefits, both in terms of biodiversity conservation and supporting human livelihoods. </jats:p>

<jats:title>Restoring Oysters</jats:title> <jats:p> Populations and wild fisheries of native oyster species have collapsed worldwide because of overfishing and habitat destruction, resulting in severe ecosystem alteration and degradation. Expensive restoration efforts have met with little success, leading to the introduction of non-native oyster species in an attempt to recover lost economic and ecological benefits. In the Chesapeake Bay on the U.S. East Coast, eastern oyster landings and population abundance have plummeted to approximately 1% of historical levels, despite considerable expensive attempts to restore the fishery. <jats:bold> Schulte <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="1124" related-article-type="in-this-issue" vol="325" xlink:href="10.1126/science.1176516">1124</jats:related-article> , published online 30 July) present field evidence of a successful restoration of a large metapopulation of native oysters in the Great Wicomico River, a tributary on the western shore of the Chesapeake Bay. The metapopulation is composed of a network of reef complexes spanning 35 hectares and comprises an estimated 185 million live native oysters of 1-year-old juveniles and 2- and 3-year-old adults. </jats:p>

<jats:title>Hidden Pockets of Resistance</jats:title> <jats:p> Groups of bacteria indulge in gene swapping at frequencies correlated with prevailing selection pressures and phylogenetic relatedness. When assaulted by antibiotics, antibiotic resistance genes become favored currency for exchange among bacteria. During sequencing of human gut microflora, <jats:bold> Sommer <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="1128" related-article-type="in-this-issue" vol="325" xlink:href="10.1126/science.1176950">1128</jats:related-article> ) found a very large reservoir of distinct genes that, when put into <jats:italic>Escherichia coli</jats:italic> , conferred resistance to a wide range of drugs. By contrast, analysis of the culturable aerobic gut microbiome, which constitutes a tiny fraction of the entire gut flora, revealed resistance genes highly similar to those harbored by human pathogens. Although there is a risk of novel modes of antibiotic resistance emerging from this reservoir, because they are evolutionarily distant, gene transfer between pathogens and the poorly known majority of the microbiome might actually be quite restricted. </jats:p>

<jats:title>Beat It</jats:title> <jats:p> Primary cilia are specialized organelles that serve important sensory functions in many different tissues and cells, and defects in their structure and function underlie a variety of genetic diseases. In contrast to primary cilia, motile cilia serve a mechanical function. For example, the cilia on airway epithelia remove inhaled material from the lung. <jats:bold> Shah <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="1131" related-article-type="in-this-issue" vol="325" xlink:href="10.1126/science.1173869">1131</jats:related-article> , published online 23 July; see the cover; see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="5944" page="1081" related-article-type="in-this-issue" vol="325" xlink:href="10.1126/science.1179180">Kinnamon and Reynolds</jats:related-article> </jats:bold> ) now show that these classic motile cilia are also chemosensory. The motile cilia on airway epithelia contain bitter-taste receptors and their associated signaling machinery. Moreover, application of bitter substances triggers an elevation of intracellular Ca <jats:sup>2+</jats:sup> levels and increases cilia beat frequency. Thus, in airway epithelia, bitter-taste receptors may be able to detect noxious substances entering the airways and initiate an autonomous defensive mechanism designed to accelerate elimination of the offending compound. </jats:p>

<jats:title>Regulating Akt</jats:title> <jats:p> The protein kinase Akt is activated in response to receptor-activated generation of the signaling second messenger phosphatidylinositol 3,4,5-trisphosphate and has roles in regulation of diverse processes from metabolism and cell survival to transcription and tumorigenesis. <jats:bold> Yang <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="1134" related-article-type="in-this-issue" vol="325" xlink:href="10.1126/science.1175065">1134</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="5944" page="1083" related-article-type="in-this-issue" vol="325" xlink:href="10.1126/science.1179972">Restuccia and Hemmings</jats:related-article> </jats:bold> ) report a previously unrecognized mode of regulation of Akt: covalent modification of Akt by linkage to lysine 63 of ubiquitin molecules. Such ubiquitination of Akt promotes localization to the cell membrane and consequent activation in cells stimulated with growth factors. TRAF6 (TNF receptor–associated factor 6) was implicated as the E3 ubiquitin ligase that mediates ubiquitination of Akt. Ubiquitination of Akt may influence its role in cancer cells: A mutant form of Akt associated with human cancer showed increased ubiquitination, and depletion of TRAF6 decreased tumorigenicity of a prostate cancer cell line in a mouse cancer model. </jats:p>

<jats:title>Tapping the Mitochondrial Proteome</jats:title> <jats:p> Mitochondria produce the energy that cells need to survive, function, and divide. A growing list of human disorders has been traced to defects in mitochondrial function. About 300 mammalian mitochondrial proteins are functionally uncharacterized, and <jats:bold> Hao <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="325" xlink:href="10.1126/science.1175689">1139</jats:related-article> , published online 23 July) reasoned that the most highly conserved proteins within this group might provide insights into human disease. A combination of bioinformatics, yeast genetics, biochemistry, and human genetics was used to show that a previously uncharacterized mitochondrial protein (Sdh5) is required for the activity of respiratory complex II. Inactivating mutations in the human gene encoding <jats:italic>SDH5</jats:italic> were found in individuals with hereditary paraganglioma, a rare neuroendocrine tumor. Thus, analysis of a mitochondrial protein in yeast has revealed a human tumor susceptibility gene. </jats:p>

<jats:title> T <jats:sub>reg</jats:sub> Responses to Eos </jats:title> <jats:p> CD4 <jats:sup>+</jats:sup> regulatory T cells (T <jats:sub>regs</jats:sub> ) are critical for keeping our immune system in check: They prevent immune responses from getting out of hand and keep autoimmunity at bay. By activating the expression of some genes and turning off expression of others, the master regulatory transcription factor of T <jats:sub>regs</jats:sub> , Foxp3, endows these cells with the appropriate gene expression program to mediate their suppressive effects. <jats:bold> Pan <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="1142" related-article-type="in-this-issue" vol="325" xlink:href="10.1126/science.1176077">1142</jats:related-article> , published online 20 August) now demonstrate that the transcription factor Eos is selectively required for Foxp3-mediated gene suppression in mice. Genes normally suppressed by Foxp3 in T <jats:sub>regs</jats:sub> remained “on” when Eos expression was suppressed, whereas genes activated by Foxp3 were unaffected. T <jats:sub>reg</jats:sub> function was also affected by Eos suppression. With half their genetic program disrupted, these cells resembled an intermediate between T <jats:sub>regs</jats:sub> and conventional CD4 <jats:sup>+</jats:sup> T cells—unable to suppress immune responses properly and partially responsive to T cell–activating stimulation. </jats:p>

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