Catálogo de publicaciones - revistas

<jats:title>Mother Knows Best</jats:title> <jats:p> Fruit flies feed on decomposing fruit, a food source rich in alcohol, and thus have evolved a high alcohol tolerance not shared by many other species. High levels of ingested alcohol protect fly larvae against parasitic wasp larvae. <jats:bold> Kacsoh <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="6122" page="947" related-article-type="in-this-issue" vol="339" xlink:href="10.1126/science.1229625">947</jats:related-article> ) show that this therapeutic use of alcohol to combat a parasite has an intergenerational component. When fly mothers were permitted to see parasitic wasps, they preferentially laid their eggs on substrates containing high alcohol levels as a way to medicate their offspring against potential infection. </jats:p>

<jats:title>Pressing Pause</jats:title> <jats:p> The pausing of RNA polymerase II (Pol II) near promoters is an important and distinct regulatory step in the process of transcribing DNA into RNA. Although protein factors and DNA elements involved in pausing have been identified, the post-initiation events that lead to pausing are poorly understood. <jats:bold> Kwak <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="6122" page="950" related-article-type="in-this-issue" vol="339" xlink:href="10.1126/science.1229386">950</jats:related-article> ) present an approach, termed PRO-seq, for monitoring the position of actively transcribing RNA polymerase with single-nucleotide precision. The approach was used to explore the mechanism of promoter proximal pausing and showed that precise positioning between core promoter elements and the pause site is critical. The findings show how the promoter dictates transcriptional pausing and detects the preferential localization of active transcription complexes within the genome. </jats:p>

<jats:title>Assessing Singletons</jats:title> <jats:p> The one-child policy introduced by the government of China in 1979 increased the proportion of urban families with an only child; later referred to as "little emperors" in media reports. In 2010, <jats:bold> Cameron <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="6122" page="953" related-article-type="in-this-issue" vol="339" xlink:href="10.1126/science.1230221">953</jats:related-article> , published online 10 January) recruited approximately 400 residents of Beijing who had been born either before the implementation of the policy (1975 and 1978) or after (1980 and 1983). Using economic games to measure trust, risk, and willingness to compete, they found that the post-1979 cohorts were less trusting and less willing to compete and also more risk averse. </jats:p>

<jats:title>Promoter Mutations and Cancer</jats:title> <jats:p> Cancer genome sequencing projects have highlighted the pathogenic role of recurrent mutations within the protein-coding regions of genes. Now, two studies suggest that the scope of mutations in human tumors extends to gene regulatory regions. In a study of 70 melanomas, <jats:bold> Huang <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="6122" page="957" related-article-type="in-this-issue" vol="339" xlink:href="10.1126/science.1229259">957</jats:related-article> , published online 24 January) found that 71% harbored one of two specific mutations in the promoter region of <jats:italic>TERT</jats:italic> , the gene coding for the catalytic subunit of telomerase, the enzyme that caps chromosome ends. Independently, <jats:bold> Horn <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="6122" page="959" related-article-type="in-this-issue" vol="339" xlink:href="10.1126/science.1230062">959</jats:related-article> , published online 24 January) identified a disease-segregating germline mutation in the <jats:italic>TERT</jats:italic> promoter in a family predisposed to melanoma and found additional <jats:italic>TERT</jats:italic> promoter mutations in a high percentage of sporadic melanomas and melanoma cell lines. The mutations in both studies generated new binding sites for specific transcription factors and, in reporter assays, caused an increase in transcription. </jats:p>

<jats:title>Promoter Mutations and Cancer</jats:title> <jats:p> Cancer genome sequencing projects have highlighted the pathogenic role of recurrent mutations within the protein-coding regions of genes. Now, two studies suggest that the scope of mutations in human tumors extends to gene regulatory regions. In a study of 70 melanomas, <jats:bold> Huang <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="6122" page="957" related-article-type="in-this-issue" vol="339" xlink:href="10.1126/science.1229259">957</jats:related-article> , published online 24 January) found that 71% harbored one of two specific mutations in the promoter region of <jats:italic>TERT</jats:italic> , the gene coding for the catalytic subunit of telomerase, the enzyme that caps chromosome ends. Independently, <jats:bold> Horn <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="6122" page="959" related-article-type="in-this-issue" vol="339" xlink:href="10.1126/science.1230062">959</jats:related-article> , published online 24 January) identified a disease-segregating germline mutation in the <jats:italic>TERT</jats:italic> promoter in a family predisposed to melanoma and found additional <jats:italic>TERT</jats:italic> promoter mutations in a high percentage of sporadic melanomas and melanoma cell lines. The mutations in both studies generated new binding sites for specific transcription factors and, in reporter assays, caused an increase in transcription. </jats:p>

<jats:title>Cost-Benefit of ART</jats:title> <jats:p> In the battle to control HIV, mass antiretroviral treatment (ART) costs $500 to $900 per person per year. <jats:bold> Bor <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="6122" page="961" related-article-type="in-this-issue" vol="339" xlink:href="10.1126/science.1230413">961</jats:related-article> ) calculated the impact of intensifying ART on the life expectancy of people living in rural KwaZulu Natal. The dates of death were collected from a population of about 100,000 people during 2000–2011: Four years before and 8 years after the scaling up of ART. Life expectancy of adults increased by more than 11 years after ART was expanded, and the economic value of the lifetimes gained were calculated to far exceed the cost of treatment. <jats:bold> Tanser <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="6122" page="966" related-article-type="in-this-issue" vol="339" xlink:href="10.1126/science.1228160">966</jats:related-article> ) followed nearly 17,000 HIV-uninfected individuals in KwaZulu-Natal over an 8-year period. Holding other HIV risk factors constant, individual HIV acquisition risk declined significantly with increasing ART coverage of HIV-infected people. </jats:p>

<jats:title>Cost-Benefit of ART</jats:title> <jats:p> In the battle to control HIV, mass antiretroviral treatment (ART) costs $500 to $900 per person per year. <jats:bold> Bor <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="6122" page="961" related-article-type="in-this-issue" vol="339" xlink:href="10.1126/science.1230413">961</jats:related-article> ) calculated the impact of intensifying ART on the life expectancy of people living in rural KwaZulu Natal. The dates of death were collected from a population of about 100,000 people during 2000–2011: Four years before and 8 years after the scaling up of ART. Life expectancy of adults increased by more than 11 years after ART was expanded, and the economic value of the lifetimes gained were calculated to far exceed the cost of treatment. <jats:bold> Tanser <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="6122" page="966" related-article-type="in-this-issue" vol="339" xlink:href="10.1126/science.1228160">966</jats:related-article> ) followed nearly 17,000 HIV-uninfected individuals in KwaZulu-Natal over an 8-year period. Holding other HIV risk factors constant, individual HIV acquisition risk declined significantly with increasing ART coverage of HIV-infected people. </jats:p>

<jats:title>Stealth Delivery</jats:title> <jats:p> Delivery of therapeutics and imaging agents is hampered by the ability of the innate immune system to recognize and clear foreign particles. "Self" cells are protected from phagocytic clearance by the membrane protein CD47 that interacts with signal regulatory protein-α (SIRPα) on macrophages. Taking advantage of this protective strategy, <jats:bold> Rodriguez <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="6122" page="971" related-article-type="in-this-issue" vol="339" xlink:href="10.1126/science.1229568">971</jats:related-article> ) labeled nanoparticles with computationally designed minimal human-CD47–based peptide (hCD47). When injected into a strain of mice in which macrophages expressed a SIRPα that cross-reacts with hCD47, the peptide prevented clearance of nanoparticles and enhanced drug delivery to tumors. </jats:p>

<jats:title>Caspase-11–Dependent Pyroptosis</jats:title> <jats:p> Inflammasomes are multiprotein complexes that assemble to initiate immunity to a variety of microorganisms, as well as to sterile tissue injury. Although a role for caspase-1 downstream of inflammasomes is well characterized, the discovery that caspase-1 knockout mice were also deficient in caspase-11 has led to a reassessment of the function of caspase-11. <jats:bold> Aachoui <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="6122" page="975" related-article-type="in-this-issue" vol="339" xlink:href="10.1126/science.1230751">975</jats:related-article> , published online 24 January; see the Perspective by <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6122" page="912" related-article-type="in-this-issue" vol="339" xlink:href="10.1126/science.1235639"> <jats:bold>Cemma and Brumell</jats:bold> ) </jats:related-article> now demonstrate that caspase-11 is required for immunity against cytosolic bacteria in mice. Only bacteria that were able to access cytosol-activated caspase-11–dependent pyroptosis, an inflammatory type of cell death. This function of caspase-11 appeared to be independent of canonical inflammasomes. </jats:p>

<jats:p>Listen to stories on the cost-effectiveness of HIV treatment, nuclear testing in North Korea, preserving plant diversity, and more.</jats:p>