Catálogo de publicaciones - revistas

<jats:title>Lipid Kinase Revealed</jats:title> <jats:p> The lipid kinase, Vps34, makes the key signaling lipid phosphatidylinositol 3-phosphate [PI(3)P] and has essential roles in autophagy, membrane trafficking, and cell signaling. It is a class III PI 3-kinase, a class against which there is currently no specific inhibitor. <jats:bold> Miller <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="1638" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1184429">1638</jats:related-article> ) now describe the crystal structure of Vps34. Modeling substrate binding and combining structural data with mutagenesis suggests a mechanism in which Vps34 is auto-inhibited in solution, but adopts a catalytically active conformation on membranes. Structures of Vps34 with existing inhibitors might allow for the generation of inhibitors with high affinity and specificity. </jats:p>

<jats:title>Trophic Trade-Offs</jats:title> <jats:p> There have been many attempts to document and explain the effects of predators on plant biomass in so-called “trophic cascades.” Theory suggests that fast-growing plants are relatively undefended and suffer more from herbivory, which implies a functional trade-off between investment in traits relating to growth and defensive strategies. <jats:bold> Mooney <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="1642" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1184814">1642</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="5973" page="1583" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1187724">Hambäck</jats:related-article> </jats:bold> ) compared responses to fertilization and aphid predators in 16 milkweed species. As predicted, interspecific variation in the strength of top-down control in terms of a tradeoff with growth was observed. </jats:p>

<jats:title>Mosquito Double Act</jats:title> <jats:p> Peroxidase/dual oxidase (duox) systems act in concert to catalyze the nonspecific formation of dityrosine bonds, which cross-link a variety of proteins. Knowing that these reactions are involved in fine-tuning insect immune responses, <jats:bold> Kumar <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="1644" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1184008">1644</jats:related-article> , published online 11 March) investigated how the peroxidase/duox system in malaria-vector mosquitoes protects the gut flora by modulating midgut antibacterial responses. Generating immune reactions resulted in a loss of mosquito egg viability, but modulating host responses allowed malaria parasites to persist among the surviving commensal flora. The peroxidase/duox system appears to promote dityrosine bond formation between proteins across the surface of midgut epithelial cells to form a layer that inhibits immune recognition and mediator release. Interference with the formation of this layer might provide a target for mosquito and malaria control. </jats:p>

<jats:title>The Making of the Males</jats:title> <jats:p> Most plants have a hermaphroditic mating system with flowers with both male and female function. However, in some cases, species are invaded by a sex-specific sterility factor. When female sterility factors invade a population, it results in a mating system called androdioecy. Theoretically, these female sterile (male) individuals should occur at low frequencies because of their reduced reproductive capacity. However, some species in the olive family have a greater than expected frequency of males. <jats:bold> Saumitou-Laprade <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="1648" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1186687">1648</jats:related-article> ) show that, for one species, males were able to reach high frequencies because of the retention of a self-incompatibility factor within hermaphroditic individuals. In this case, hermaphroditic individuals can only mate with individuals outside of their incompatibility type, reducing their available mating partners, whereas males are able to mate with all hermaphrodites. This explains how, contrary to theory, high frequencies of males can exist within populations. </jats:p>

<jats:title>A Pathway to Leukemia</jats:title> <jats:p> Leukemia is initiated and maintained by a small number of self-renewing cells called leukemia stem cells (LSCs), which share properties with hematopoietic stem cells (HSCs), the self-renewing cells that produce healthy blood cells. <jats:bold> Wang <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="1650" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1186624">1650</jats:related-article> ) studied mouse models of acute myelogenous leukemia (AML), a disease that is often refractory to existing therapies. Activation of the Wnt/β-catenin signaling pathway was required for efficient oncogene-mediated conversion of HSCs into LSCs. This pathway is among the most well studied signaling pathways in cell biology, setting the stage for testing of β-catenin signaling antagonists in preclinical models of AML. </jats:p>

<jats:title>Heart Cell Signaling in 3D</jats:title> <jats:p> A healthy heart relies on the proper transduction of cellular signals through the β <jats:sub>1</jats:sub> - and β <jats:sub>2</jats:sub> -adrenergic receptors (βARs), which are located on the surface of the heart's muscle cells (cardiomyocytes). The surface of these cells resembles a highly organized series of hills and valleys and it has been unclear whether this topography plays a role in the βAR signaling events that are critical to cell function. <jats:bold> Nikolaev <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="1653" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1185988">1653</jats:related-article> , published online 25 February; see Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="5973" page="1586" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1188538">Dorn</jats:related-article> </jats:bold> ) monitored the cyclic adenosine monophosphate (cAMP) signals generated by the βARs in living cardiomyocytes. In cells from healthy rats and from rats with heart failure, the β <jats:sub>1</jats:sub> ARs were localized across the entire cell surface. In contrast, the spatial localization of the β <jats:sub>2</jats:sub> ARs differed in healthy and failing cells. In healthy cardiomyocytes, the β <jats:sub>2</jats:sub> ARs resided exclusively within surface invaginations called transverse tubules, thereby producing spatially confined cAMP signals, whereas in failing cardiomyocytes, the β <jats:sub>2</jats:sub> ARs redistributed to other cell surface areas, thereby producing diffuse cAMP signals. Thus, changes in the spatial localization of β <jats:sub>2</jats:sub> AR-induced cAMP signaling may contribute to heart failure. </jats:p>

<jats:title>Shelterin the Ends</jats:title> <jats:p> The ends of linear chromosomes suffer two problems: They cannot be replicated to their termini, resulting in loss of terminal sequences; and they can be mistakenly sensed as DNA double-strand breaks, activating DNA repair pathways that can result in serious genome derangement. These problems are solved by the addition of telomeres, repeat sequences at the ends of chromosomes, which are shielded by a protein complex called shelterin. <jats:bold> Sfeir <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="1657" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1185100">1657</jats:related-article> ) show that the mouse Rap1 protein, which is part of the shelterin complex and which binds to a second shelterin protein called TRF2, helps prevent telomeres undergoing unscheduled homologous recombination. Such recombination could threaten telomere integrity by generating sequence exchanges between sister telomeres resulting in critically shortened telomeres. </jats:p>

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