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<jats:title>Biodiversity and Productivity</jats:title> <jats:p> When data are analyzed at relatively large spatial scales, biodiversity generally increases with productivity, but the pattern at smaller scales is more variable. <jats:bold>Chase</jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="1388" related-article-type="in-this-issue" vol="328" xlink:href="10.1126/science.1187820">1388</jats:related-article> , published online 27 May) presents results from a 7-year experiment in artificial ponds. β-diversity (the variation in species composition from site to site) in animal species was persistently higher at higher productivity among otherwise homogeneous environments in this controlled experimental venue. This pattern appeared to result from shifts in the relative importance of deterministic versus stochastic community assembly mechanisms along the productivity gradient. Thus, variation in the mechanism of community assembly might be an important process determining the relationship between biodiversity and productivity. </jats:p>

<jats:title>The Inner Life</jats:title> <jats:p> The influence of intestinal flora on the physiology of the entire host organism has only recently begun to be appreciated. The mammalian gut is not just home to billions of bacteria and archaea, but often harbors much larger creatures such as protozoa, nematodes, and tapeworms. Anticipating a web of interactions among these organisms, <jats:bold> Hayes <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="1391" related-article-type="in-this-issue" vol="328" xlink:href="10.1126/science.1187703">1391</jats:related-article> ) investigated the relationship between a common nematode parasite of mice, <jats:italic>Trichuris muris</jats:italic> , and its dependency on the occurrence of enterobacteria, such as <jats:italic>Escherichia coli</jats:italic> and <jats:italic>Salmonella typhimurium</jats:italic> . The worms were found to be dependent on the presence of bacteria for hatching, and hatching was triggered by the presence of bacterial surface structures called fimbriae, which bind to proteins at the poles of the worms' eggs. </jats:p>

<jats:title>Not GILT-Free Processing</jats:title> <jats:p> CD8 <jats:sup>+</jats:sup> T cells respond to infections by recognizing peptide antigens bound to major histocompatability complex class I (MHC class I) protein expressed on the surface of antigen-presenting cells (APCs). Because MHC class I can only present intracellular antigens, antigen cross-presentation is important for responses to viruses that do not directly infect APCs. Antigen cross-presentation occurs when APCs acquire antigens by phagocytosis of dying virally infected cells and present them to CD8 <jats:sup>+</jats:sup> T cells. After internalization, antigens must enter the cytosol for processing by the proteasome. <jats:bold>Singh and Cresswell</jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="1394" related-article-type="in-this-issue" vol="328" xlink:href="10.1126/science.1189176">1394</jats:related-article> ) now show that GILT (gamma-interferon–inducible lysosomal thiolreductase) is required for cross-presentation in mice of disulfide-containing viral antigens. In mice lacking GILT, the CD8 <jats:sup>+</jats:sup> T cell response to antigens derived from disulfide-rich proteins was substantially impaired after influenza A or herpes simplex virus 1 infection. Thus, cross-presentation of some antigens requires an early processing step prior to proteasomal degradation in the cytosol and subsequent MHC class I loading. </jats:p>

<jats:title>Chloride Balancing Act</jats:title> <jats:p> The ionic composition of the cytosol and intracellular organelles must be regulated in the face of ongoing membrane traffic into and out of the cell. Now, two papers address the consequences of a change in the transport phenotype of an intracellular Cl <jats:sup>−</jats:sup> transport protein from a coupled exchanger to a passive Cl <jats:sup>−</jats:sup> conductor (see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="5984" page="1364" related-article-type="in-this-issue" vol="328" xlink:href="10.1126/science.1191529">Smith and Schwappach</jats:related-article> </jats:bold> ). <jats:bold> Novarino <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="1398" related-article-type="in-this-issue" vol="328" xlink:href="10.1126/science.1188070">1398</jats:related-article> , published online 29 April) investigated the consequence of a knock-in of the uncoupled ClC-5 transporter into mouse. The knock-out mouse of this endosomal kidney transporter has a severe endocytic phenotype believed to be due to a defect in vesicular acidification. The current study shows a similarly impaired endocytic phenotype for the uncoupled mutant, but the acidification of endosomes was unaffected. <jats:bold> Weinert <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="1401" related-article-type="in-this-issue" vol="328" xlink:href="10.1126/science.1188072">1401</jats:related-article> , published online 29 April) used a similar strategy to investigate the consequence of the equivalent mutation in the lysosomal transporter ClC-7, which is highly expressed in the resorption lacuna of osteoclasts and whose knock-out in mice produces lysosomal storage disease and severe osteopetrosis. A similar (though less severe) phenotype was observed in the knock-in mice containing the uncoupled ClC-7, indicating that coupled transport plays a critical role in lysosomes. </jats:p>

<jats:title>Chloride Balancing Act</jats:title> <jats:p> The ionic composition of the cytosol and intracellular organelles must be regulated in the face of ongoing membrane traffic into and out of the cell. Now, two papers address the consequences of a change in the transport phenotype of an intracellular Cl <jats:sup>−</jats:sup> transport protein from a coupled exchanger to a passive Cl <jats:sup>−</jats:sup> conductor (see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="5984" page="1364" related-article-type="in-this-issue" vol="328" xlink:href="10.1126/science.1191529">Smith and Schwappach</jats:related-article> </jats:bold> ). <jats:bold> Novarino <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="1398" related-article-type="in-this-issue" vol="328" xlink:href="10.1126/science.1188070">1398</jats:related-article> , published online 29 April) investigated the consequence of a knock-in of the uncoupled ClC-5 transporter into mouse. The knock-out mouse of this endosomal kidney transporter has a severe endocytic phenotype believed to be due to a defect in vesicular acidification. The current study shows a similarly impaired endocytic phenotype for the uncoupled mutant, but the acidification of endosomes was unaffected. <jats:bold> Weinert <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="1401" related-article-type="in-this-issue" vol="328" xlink:href="10.1126/science.1188072">1401</jats:related-article> , published online 29 April) used a similar strategy to investigate the consequence of the equivalent mutation in the lysosomal transporter ClC-7, which is highly expressed in the resorption lacuna of osteoclasts and whose knock-out in mice produces lysosomal storage disease and severe osteopetrosis. A similar (though less severe) phenotype was observed in the knock-in mice containing the uncoupled ClC-7, indicating that coupled transport plays a critical role in lysosomes. </jats:p>

<jats:title>Seeing EPO</jats:title> <jats:p> The supply of red blood cells in mammals is controlled by the cytokine erythropoietin (EPO). In physiological situations, the concentration of EPO can change by 1000-fold. <jats:bold> Becker <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="1404" related-article-type="in-this-issue" vol="328" xlink:href="10.1126/science.1184913">1404</jats:related-article> , published online 20 May) used a combination of mathematical modeling and experimental analysis to discern how cells can maintain a linear response to such a broad range of EPO concentrations. Critical features included internalization of EPO-bound receptors and subsequent degradation of the EPO ligand. Replenishment of receptors at the cell surface required a large supply of EPO receptors maintained in reserve inside the cell. These mechanisms allow cells to experience large increases in EPO concentration without becoming refractory to further stimulation. </jats:p>

<jats:title>Oxytocin and Intergroup Conflict</jats:title> <jats:p> Human society is organized into groups, such as those based on nationality or religion, which can lead to intergroup conflicts, with sometimes devastating consequences. Intergroup conflict engages a human behavior termed parochial altruism: For example, a soldier who fights against the enemy at risk to themselves to protect their country is a parochial altruist. <jats:bold> De Dreu <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="1408" related-article-type="in-this-issue" vol="328" xlink:href="10.1126/science.1189047">1408</jats:related-article> ; see the cover; see the News story by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="5984" page="1343-a" related-article-type="in-this-issue" vol="328" xlink:href="10.1126/science.328.5984.1343-a">Miller</jats:related-article> </jats:bold> ) have discovered a role for oxytocin, a neuropeptide produced in the hypothalamus, in regulating parochial altruism during human intergroup competition and conflict. Oxytocin is already known to play a role in trusting behavior, and naturally occurring genetic variants of the oxytocin receptor exist within the human population. Administration of oxytocin modulated defense-related aggression toward competing groups, but did not affect unprovoked, hateful behavior. Thus, there may be a neurobiological basis for intergroup conflict in humans. </jats:p>

<jats:title>Lost in a Maze</jats:title> <jats:p> In rodents, hippocampal CA1 neurons play a pivotal role in the processing of spatial memory. However, the contribution of CA1 neurons in the human hippocampus to spatial memory has been difficult to establish. <jats:bold> Bartsch <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="1412" related-article-type="in-this-issue" vol="328" xlink:href="10.1126/science.1188160">1412</jats:related-article> ) studied a group of patients with transient global ischemia, a condition that lasted for at most a few hours and was followed by complete recovery. The patients were tested on a range of complex neuropsychological instruments, including virtual reality, during the ischemic attack. A striking impairment was observed in simple spatial navigation to a hidden target. The performance of the patients was correlated with the duration of the transient global ischemia, as well as with the size of the CA1 lesions. </jats:p>

<jats:title>Too Much of a Good Thing</jats:title> <jats:p> In peripheral nerves, the insulating myelin sheath speeds up electrical conductivity by allowing impulses to skip down the axon from node to node. Axons signal using neuregulin to get the Schwann cells to begin their wrap-around insulation project. But when is enough myelin too much? <jats:bold> Cotter <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="1415" related-article-type="in-this-issue" vol="328" xlink:href="10.1126/science.1187735">1415</jats:related-article> , published online 6 May) have now found the signal that stops further rounds of myelin insulation. In developing mice, the proteins Dlg1 (mammalian disc large 1) and PTEN (phosphatase and tensin homolog) were involved in calling a halt to insulation during early development. The balance between not enough and too much myelin insulation is controlled by opposing signals, which together optimize both the myelination and the velocity of nerve conduction. </jats:p>

<jats:p>The show includes oxytocin's role in parochial altruism, the origins of Oort cloud comets, evidence that Polynesians sailed to South America, and more.</jats:p>