Catálogo de publicaciones - revistas

<jats:title>Viral Superspreaders</jats:title> <jats:p> Viruses are thought to spread across a lawn of cells by an iterative process of infection, replication, and release. If this were the case, the rate of spread would be limited by the viral replication kinetics. Now, <jats:bold> Doceul <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="873" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1183173">873</jats:related-article> , published online 21 January; see the Perspective by <jats:bold>Pickup</jats:bold> ) describe a spreading mechanism used by vaccinia virus that is not restricted by viral replication kinetics and that causes a dramatic acceleration of spread. Early after infection, vaccinia virus proteins A33 and A36 are expressed as a complex on the cell surface. This marks the cell as infected and causes superinfecting virions to be repelled by the formation of actin projections beneath the virus particle. Virions are repelled from infected cells repeatedly until an uninfected cell is reached and are thus pushed further away from the origin of infection to accelerate dissemination. </jats:p>

<jats:title>Homing in on Hotspots</jats:title> <jats:p> The clustering of recombination in the genome, around locations known as hotspots, is associated with specific DNA motifs. Now, using a variety of techniques, three studies implicate a chromatin-modifying protein, the histone-methyltransferase PRDM9, as a major factor involved in human hotspots (see the Perspective by <jats:bold> Cheung <jats:italic>et al.</jats:italic> </jats:bold> ). <jats:bold> Parvanov <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="835" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1181495">835</jats:related-article> , published online 31 December) mapped the locus in mice, and analyzed allelic variation in mice and humans, whereas <jats:bold> Myers <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="876" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1182363">876</jats:related-article> , published online 31 December) used a comparative analysis between human and chimpanzees to show that the recombination process leads to a self-destructive drive in which the very motifs that recruit hotspots are eliminated from our genome. <jats:bold> Baudat <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="836" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1183439">836</jats:related-article> , published online 31 December) took this analysis a step further to identify human allelic variants within Prdm9 that differed in the frequency at which they used hotspots. Furthermore, differential binding of this protein to different human alleles suggests that this protein interacts with specific DNA sequences. Thus, PDRM9 functions in the determination of recombination loci within the genome and may be a significant factor in the genomic differences between closely related species. </jats:p>

<jats:title>It's All About Self-Renewal</jats:title> <jats:p> The <jats:italic>Lmo2</jats:italic> oncogene was identified as a contributing factor in human T cell acute lymphoblastic leukemia (T-ALL) nearly two decades ago, but the gene rose to prominence in 2003 when its inadvertent activation by a retroviral vector was shown to cause leukemia in two patients in a gene therapy trial. The cellular mechanism by which the gene product of <jats:italic>Lmo2</jats:italic> , a transcriptional regulator, induces T-ALL is poorly understood. Studying transgenic mice, <jats:bold> McCormack <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="879" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1182378">879</jats:related-article> , published online 21 January) now show that <jats:italic>Lmo2</jats:italic> confers self-renewal activity to committed T cells in the thymus without affecting their capacity for T cell differentiation. These self-renewing cells, which were detectable 8 months prior to the onset of overt leukemia in the mice, expressed genes in common with hematopoietic stem cells (HSCs), suggesting that <jats:italic>Lmo2</jats:italic> might reactivate an HSC-specific transcriptional program. </jats:p>

<jats:title>Pinpointing Genetic Selection</jats:title> <jats:p> The human genome contains hundreds of regions with evidence of recent positive natural selection, yet, for all but a handful of cases, the underlying advantageous mutation remains unknown. Current methods to detect the signal of selection often results in the identification of a broad genomic region containing many candidate regions that vary among individuals. By combining existing statistical methods, <jats:bold> Grossman <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="883" related-article-type="in-this-issue" vol="327" xlink:href="10.1126/science.1183863">883</jats:related-article> , published online 7 January) developed a method, termed Composite of Multiple Signals, which can increase the ability to pinpoint the specific variant under selection. Several candidate regions under selection in human populations were identified. </jats:p>

<jats:p>A weekly roundup of information on newly offered instrumentation, apparatus, and laboratory materials of potential interest to researchers.</jats:p>

<jats:p>The show includes measuring food insecurity, rethinking agriculture for the 21st century, and reducing meat consumption.</jats:p>