Catálogo de publicaciones - revistas

<jats:title>The Yin and Yang of Plant Caspases</jats:title> <jats:p> The function of plant metacaspases, identified by limited sequence homology to the animal caspases that control cell death, has remained elusive. <jats:bold> Coll <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="1393" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1194980">1393</jats:related-article> ) have now elucidated the actions of two metacaspases in the small plant <jats:italic>Arabidopsis</jats:italic> . One metacaspase, AtMC1, promoted cell death, and the other, AtMC2, acted antagonistically to stall cell death. The results help to elucidate the mechanisms by which plants control cell survival during development and defend against pathogen attack. </jats:p>

<jats:title>Just Beet It</jats:title> <jats:p> Flowering time regulation is important for plants to maximize their reproductive output. By investigating copies of genes that are strong and central activators of flowering in many different species (homologs of the <jats:italic>FT</jats:italic> gene in <jats:italic>Arabidopsis</jats:italic> ), <jats:bold> Pin <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="1397" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1197004">1397</jats:related-article> ) found that during evolution, the regulation of flowering time in sugar beet ( <jats:italic>Beta vulgaris</jats:italic> ) has come under the control of two <jats:italic>FT</jats:italic> -like genes. Functional differences in these genes owing to small mutations in a critical domain have caused a duplicated copy of the flowering promoter <jats:italic>FT</jats:italic> to turn into a flowering repressor in sugar beet. These changes may explain why cultivated beets are unable to flower until their second year after passing through the winter, a behavior important for increasing crop yield. </jats:p>

<jats:title>Pain in the Brain</jats:title> <jats:p> One of the major challenges in pain research is finding ways to reverse chronic pain. Synaptic long-term potentiation (LTP) at spinal or cortical levels is a cellular model of chronic pain. <jats:bold> X.-Y. Li. <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="1400" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1191792">1400</jats:related-article> ) studied the role of the enzyme protein kinase M zeta (PKMζ) in neurons of the anterior cingulate cortex (ACC) in the maintenance of LTP and for enhanced pain sensitivity after peripheral nerve injury in mice. Nerve injury appeared to lead to the up-regulation and phosphorylation of PKMζ. This triggered LTP at some synapses in the ACC by increasing the number of AMPA receptors. LTP was restricted to ACC neurons that were activated by nerve injury. Blocking PKMζ in the ACC days after nerve injury normalized pain behavior. Thus, PKMζ may represent a promising target for the treatment of chronic pain. </jats:p>

<jats:title>Better Brain Maps</jats:title> <jats:p> A high-resolution atlas of the complete neuronal connectivity in a whole brain should fundamentally advance our understanding of the organization and function of animal nervous systems. Now, <jats:bold> A. Li. <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="330" xlink:href="10.1126/science.1191776">1404</jats:related-article> , published online 4 November) describe an automated system, micro-optical sectioning tomography, that allowed three-dimensional mapping of the morphology and spatial location of neurons and traces of neurites in a whole, intact mouse brain. </jats:p>

<jats:title>Novel or Familiar?</jats:title> <jats:p> Amnesia is characterized by a number of memory deficits, including the apparent inability to distinguish between novel and familiar stimuli. <jats:bold> McTighe <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="330" xlink:href="10.1126/science.1194780">1408</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="6009" page="1331" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1199462">Eichenbaum</jats:related-article> </jats:bold> ) observed that the recognition memory of brain-damaged rats in a standard model of amnesia was impaired not because previously experienced objects seemed to be novel, but because objects not previously experienced seemed to be familiar. Furthermore, simply placing the animal in a visually deprived environment during the delay, reducing visual interference, completely rescued the impairment. This counterintuitive finding contradicts the predominant “multiple memory systems” model in which amnesia is usually considered and forces a reconsideration of fundamental assumptions underlying our understanding of amnesia. </jats:p>

<jats:title>An Eye on Metastasis</jats:title> <jats:p> Despite the considerable progress being made in elucidating the cell biology of metastasis, little is known about the genetic alterations that promote metastasis of human tumors, the cause of most cancer deaths. A potentially important clue now emerges from the work of <jats:bold> Harbour <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="1410" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1194472">1410</jats:related-article> , published online 4 November), who used an exome-sequencing approach to search for genetic mutations in uveal melanomas, an eye cancer associated with a high rate of fatal metastasis. Remarkably, over 80% of tumor samples with a high metastatic risk had inactivating somatic mutations in the gene encoding BAP1 (BRCA1-associated protein 1), a nuclear protein involved in controlling protein degradation. Thus, in this tumor type, mutational inactivation of BAP1 may be a key event in the acquisition of metastatic competence. </jats:p>

<jats:title>Wired for Life</jats:title> <jats:p> Syntrophic bacteria live on the metabolic by-products of a partner species. The exchange of the by-products accompanies a flow of electrons in the opposite direction that helps some species grow in conditions that would otherwise be unfavorable. In mixed anaerobic cultures of two related <jats:italic>Geobacter</jats:italic> species, <jats:bold> Summers <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="1413" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1196526">1413</jats:related-article> ) observed that one species evolved to promote the transfer of electrons directly to the other, in large aggregated cell clusters, without coupling to common anaerobic by-products such as hydrogen or formate. Selection pressures in nine parallel populations all resulted in a point mutation that truncated a protein involved in the production of small hairlike projections involved in intercellular communication—pili—and indirectly increased the expression of a <jats:italic>c</jats:italic> -type multiheme cytochrome responsible for extracellular electron transfer. The evolved aggregates were conductive, suggesting that the direct exchange of electrons between partner species is a possible alternative route to anaerobic syntrophy rather than interspecies hydrogen transfer; indeed, deleting a gene that encodes a hydrogenase involved in hydrogen transfer conferred a growth advantage in the cocultures. </jats:p>

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<jats:p>Apoptosis is a simple concept with complex underpinnings--damaged cells are prompted to self-destruct through a series of molecular events, like dominos toppling over one by one. Unraveling the mechanisms underlying apoptosis is akin to determining the role each individual domino plays in a falling cascade--one strategically placed tile can trigger a cascade of several lines, and one misplaced tile can mean a dead end in the chain reaction. Techniques that pick apart this intricate process have been rapidly advancing, now offering more than the ability to look at a single event with high throughput, multiplexing capabilities, and in vivo imaging. Future technologies aim to help scientists visualize human cellular processes in vivo to aid researchers in tailoring and monitoring treatment for a variety of diseases, especially cancer.</jats:p>