Catálogo de publicaciones - revistas

<jats:title>Genetic Epigenetics</jats:title> <jats:p> Posttranslational modifications of histone proteins have been implicated in the regulation of gene transcription in organisms ranging from yeast to humans. However, epigenetic regulators can modify multiple proteins. By mutating specific histone sites in <jats:italic>Drosophila</jats:italic> , <jats:bold> Pengelly <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="6120" page="698" related-article-type="in-this-issue" vol="339" xlink:href="10.1126/science.1231382">698</jats:related-article> ) demonstrate that mutation of lysine 27 of histone H3 causes the same transcriptional defects as those observed in mutants lacking the methyltransferase PRC2 that modifies this H3 residue. These results demonstrate the functional importance of H3-K27 methylation in Polycomb repression. Furthermore, this genetic approach may be applied to investigating numerous other metazoan-specific histone modifications. </jats:p>

<jats:title>Fixing Broken DNA</jats:title> <jats:p> Some physiological processes, such as immunoglobulin class switching and telomere attrition, result in double-stranded DNA breaks. The DNA damage repair protein, 53BP1, prevents nucleolytic processing of these breaks, but the proteins it partners with to do this are unknown (see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6120" page="652" related-article-type="in-this-issue" vol="339" xlink:href="10.1126/science.1234602">Lukas and Luka</jats:related-article> s </jats:bold> ). <jats:bold> Di Virgilio <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="6120" page="711" related-article-type="in-this-issue" vol="339" xlink:href="10.1126/science.1230624">711</jats:related-article> , published online 10 January), using mass spectroscopy–based methods, and <jats:bold> Zimmermann <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="6120" page="700" related-article-type="in-this-issue" vol="339" xlink:href="10.1126/science.1231573">700</jats:related-article> , published online 10 January), using a telomere-based assay, identify Rif1 as a 53BP1 phosphorylation- and DNA damage–dependent interaction partner. Mice with a B cell–specific deletion in Rif1 showed impaired immunoglobulin class switching. Rif1-deficient cells exhibited extensive 5′-3′ resection at DNA ends, with enhanced genetic instability. Thus, Rif1 partners with 53BP1 to promote the proper repair of double-stranded DNA breaks. </jats:p>

<jats:title>Sweet Enough to Flower</jats:title> <jats:p> In making the developmental switch from vegetative growth to flowering, plants integrate diverse information, including photoperiod, hormone signals, and carbohydrate status. <jats:bold> Wahl <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="6120" page="704" related-article-type="in-this-issue" vol="339" xlink:href="10.1126/science.1230406">704</jats:related-article> ; see the Perspective by <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6120" page="659" related-article-type="in-this-issue" vol="339" xlink:href="10.1126/science.1234601"> <jats:bold>Danielson and Frommer</jats:bold> </jats:related-article> ) analyzed the physiology of the signaling sugar trehalose-6-phosphate (T6P) in <jats:italic>Arabidopsis</jats:italic> . Quantities of T6P cycle in daily rhythms that peak toward the end of the day. T6P levels in the shoot apical meristem mirrored sucrose levels. Disruption of T6P production also disrupted expression of the <jats:italic>FLOWERING LOCUS T</jats:italic> gene, which responds in leaves to day length and generates signals that direct the meristem to initiate flowering programs. T6P production also affected the signaling pathway that links the age of the plant to flowering. By incorporating requirements for T6P signaling in the flowering induction pathways, the plant ensures that adequate carbohydrate reserves have been accumulated. Thus, T6P regulates the shift to flowering by linking carbohydrate status to day length in the leaves and to developmental age in the shoot apical meristem. </jats:p>

<jats:title> <jats:italic>E. coli</jats:italic> kNOws How to Win </jats:title> <jats:p> The harmonious existence among the various microbial inhabitants of the gut is critical for good health. However, inflammation from injury or inflammatory bowel disease, can disrupt this balance and lead to the outgrowth of particular bacteria. The outgrowth of members of the Enterobacteriaceae family, which includes <jats:italic>Escherichia coli</jats:italic> , is often observed. Because <jats:italic>E. coli</jats:italic> are facultative rather an obligate anaerobes, <jats:bold> Winter <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="6120" page="708" related-article-type="in-this-issue" vol="339" xlink:href="10.1126/science.1232467">708</jats:related-article> ) postulated that they may be able to use by-products of reactive oxygen and nitrogen species, which are produced during inflammation, for anaerobic respiration, thereby edging out other fermenting bacteria. Indeed, in two mouse models of colitis and in a model of intestinal injury, various <jats:italic>E. coli</jats:italic> strains were able to use host-derived nitrate as an energy source and outcompete mutant strains unable to do this. </jats:p>

<jats:title>Fixing Broken DNA</jats:title> <jats:p> Some physiological processes, such as immunoglobulin class switching and telomere attrition, result in double-stranded DNA breaks. The DNA damage repair protein, 53BP1, prevents nucleolytic processing of these breaks, but the proteins it partners with to do this are unknown (see the Perspective by <jats:bold> <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6120" page="652" related-article-type="in-this-issue" vol="339" xlink:href="10.1126/science.1234602">Lukas and Luka</jats:related-article> s </jats:bold> ). <jats:bold> Di Virgilio <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="6120" page="711" related-article-type="in-this-issue" vol="339" xlink:href="10.1126/science.1230624">711</jats:related-article> , published online 10 January), using mass spectroscopy–based methods, and <jats:bold> Zimmermann <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="6120" page="700" related-article-type="in-this-issue" vol="339" xlink:href="10.1126/science.1231573">700</jats:related-article> , published online 10 January), using a telomere-based assay, identify Rif1 as a 53BP1 phosphorylation- and DNA damage–dependent interaction partner. Mice with a B cell–specific deletion in Rif1 showed impaired immunoglobulin class switching. Rif1-deficient cells exhibited extensive 5′-3′ resection at DNA ends, with enhanced genetic instability. Thus, Rif1 partners with 53BP1 to promote the proper repair of double-stranded DNA breaks. </jats:p>

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