Catálogo de publicaciones - revistas

<jats:title>Accessory to Obesity?</jats:title> <jats:p> Melanocortin receptors are a family of cell membrane receptors that control diverse physiological functions. Mutations in the gene encoding melanocortin 4 receptor (MC4R) are a cause of familial early-onset obesity. <jats:bold> Asai <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6143" page="275" related-article-type="in-this-issue" vol="341" xlink:href="10.1126/science.1233000">275</jats:related-article> ) studied the function of an accessory protein for MC4R signaling, MRAP2, and found that mice genetically deficient in MRAP2 develop severe obesity. Sequencing of <jats:italic>MRAP2</jats:italic> in unrelated, severely obese humans revealed one individual with a clearly disruptive genetic variant, suggesting that <jats:italic>MRAP2</jats:italic> mutations might also be a rare cause of human obesity. In a zebrafish model, <jats:bold> Sebag <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6143" page="278" related-article-type="in-this-issue" vol="341" xlink:href="10.1126/science.1232995">278</jats:related-article> ) studied two paralogs of the MRAP2 accessory protein, one of which enhanced MC4R responsiveness to α–melanocyte-stimulating hormone, which regulates feeding and growth. </jats:p>

<jats:title>Accessory to Obesity?</jats:title> <jats:p> Melanocortin receptors are a family of cell membrane receptors that control diverse physiological functions. Mutations in the gene encoding melanocortin 4 receptor (MC4R) are a cause of familial early-onset obesity. <jats:bold> Asai <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6143" page="275" related-article-type="in-this-issue" vol="341" xlink:href="10.1126/science.1233000">275</jats:related-article> ) studied the function of an accessory protein for MC4R signaling, MRAP2, and found that mice genetically deficient in MRAP2 develop severe obesity. Sequencing of <jats:italic>MRAP2</jats:italic> in unrelated, severely obese humans revealed one individual with a clearly disruptive genetic variant, suggesting that <jats:italic>MRAP2</jats:italic> mutations might also be a rare cause of human obesity. In a zebrafish model, <jats:bold> Sebag <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6143" page="278" related-article-type="in-this-issue" vol="341" xlink:href="10.1126/science.1232995">278</jats:related-article> ) studied two paralogs of the MRAP2 accessory protein, one of which enhanced MC4R responsiveness to α–melanocyte-stimulating hormone, which regulates feeding and growth. </jats:p>

<jats:title>Zeus' Revenge</jats:title> <jats:p> Sediment-dwelling amoebae appear to have an unhappy affinity for huge viruses. Giant icosahedral Mimiviruses with genomes of the order of 1 megabase (Mb) were first identified in Acanthamoeba. Digging into antipodean sediments has once again been fruitful where <jats:bold> Philippe <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6143" page="281" related-article-type="in-this-issue" vol="341" xlink:href="10.1126/science.1239181">281</jats:related-article> ; see the cover) discovered some enormous viruses in Acanthamoeba, visible by light microscopy and having genomes up to 2.5 Mb. The Pandoraviruses are phagocytosed by target cells and, after fusing with the phagosome membrane, their contents are released into the cytoplasm where they wreak terrible havoc on its nucleus. These viruses are encased into a tegument-like envelope and lack genes for capsid proteins, and there are no genes for protein translation, adenosine triphosphate generation, or binary fission—confirming their classification as viruses. </jats:p>

<jats:title>Stem Cells in Wound Healing</jats:title> <jats:p> Although excessive numbers of stem cells (SCs) may increase the risk of cancer, elevated SC numbers may be desirable, at least transiently, for the promotion of tissue repair and regeneration. <jats:bold> Fuchs <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6143" page="286" related-article-type="in-this-issue" vol="341" xlink:href="10.1126/science.1233029">286</jats:related-article> , published online 20 June) found that mice deficient for the proapoptotic <jats:italic>Sept4</jats:italic> /ARTS gene have elevated numbers of apoptosis-resistant hair follicle SCs and display dramatic improvement in wound healing and regeneration. Inactivation of the caspase inhibitor XIAP, a direct target for the proapoptotic activity of ARTS, abrogated these phenotypes and impaired wound healing. </jats:p>

<jats:title>Background Extinction</jats:title> <jats:p> Diversity results through both the processes of species origination and extinction. However, studies of extinction have tended to focus on mass extinctions, despite the fact that the background extinction represents a greater loss in terms of the absolute number of extinct taxa. In order to identify what factors affect this rate of background extinction, <jats:bold>Quental and Marshall</jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6143" page="290" related-article-type="in-this-issue" vol="341" xlink:href="10.1126/science.1239431">290</jats:related-article> , published online 20 June) explored the dynamics of 19 mammalian clades and compared the rates of expansions and declines among taxa to expected models assuming random processes. Most clades decline to extinction in a “driven” manner—that is, faster than expected by chance alone. </jats:p>

<jats:title>Playing the Tape of Life</jats:title> <jats:p> Should the tape of life be replayed, would it produce the same music? Many influential evolutionary biologists, notably Stephen J. Gould, have argued that the answer is “no.” However, patterns of convergence among different species filling similar niches all over the world have argued that the answer is neither so simple nor perhaps so negative. Classic cases of convergence, such as marsupials on the Australian continent or cichlids across the African rift lakes, have demonstrated that similar ecological pressures can result in species with similar ecological traits. Such classic examples, however, do not allow for the influence of niche filling based purely on chance. <jats:bold> Mahler <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6143" page="292" related-article-type="in-this-issue" vol="341" xlink:href="10.1126/science.1232392">292</jats:related-article> ) take advantage of the well-studied species clades of Caribbean anoles to examine patterns of adaptation and niche filling across species and islands. Across-islands convergence on a few distinct adaptive peaks (or niches) has driven diversification of species. Anomalies from these ecotypes are only found on the largest, most diverse islands. Thus, ecological niches powerfully shape species and convergence on particular forms is an inherent component of adaptation. Thus, it seems that the tape of life might play the same music, despite being produced by different instruments. </jats:p>

<jats:title>Digoxin Dangers</jats:title> <jats:p> A proportion of patients treated with digoxin, a cardiac glycoside used to treat heart function abnormalities, generate the inactive metabolite, dihydrodigoxin, resulting in poor efficacy. <jats:bold> Haiser <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6143" page="295" related-article-type="in-this-issue" vol="341" xlink:href="10.1126/science.1235872">295</jats:related-article> ) examined a potential culprit responsible for this transformation—the actinobacterium, <jats:italic>Eggerthella lenta</jats:italic> —to probe the microbiota-digoxin interaction. Microbe growth was promoted by arginine, and differential expression analysis revealed a two-gene cardiac glycoside reductase ( <jats:italic>cgr</jats:italic> ) operon that was induced by digoxin in low arginine conditions. Not all strains of <jats:italic>E. lenta</jats:italic> could reduce digoxin and, when fecal samples from healthy people were tested, a spectrum of digoxin inactivation was detected. When the digoxin-reducing strain of <jats:italic>E. lenta</jats:italic> was given to germ-free mice that were fed a high-protein (that is, high-arginine) diet, digoxin levels stayed high in serum, and drug inactivation was suppressed. </jats:p>

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<jats:title>Not mTORCing</jats:title> <jats:p> Inhibition of the protein kinase complex mTORC1 has potentially beneficial therapeutic affects that include inhibition of cancer and extension of life span. However, effects of its inhibition in vivo have sometimes been disappointing. One reason may be that the well-studied inhibitor of mTORC1, rapamycin, inhibits some effects of mTORC1 but not others. In line with this idea, <jats:bold> Kang <jats:italic>et al.</jats:italic> </jats:bold> ( <jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="uri" xlink:href="http://www.sciencemag.org/content/341/6144/1236566.full">1236566</jats:ext-link> ) show that the effect of rapamycin depends on the substrate. Characteristics of the phosphorylation sites on various substrates caused them to be phosphorylated with different efficiency by mTORC1. The substrates that were most efficiently phosphorylated were resistant to inhibition of mTORC1. The results explain how various sites, sometimes within the same protein, can differ in their sensitivity to rapamycin. </jats:p>