Catálogo de publicaciones - revistas

<jats:title>Genomic plasticity during brain development</jats:title> <jats:p> Mice genomes contain many mobile retrotransposons. Bedrosian <jats:italic>et al.</jats:italic> analyzed DNA from the mouse hippocampus during development (see the Perspective by Song and Gleeson). They found that the amount of maternal care in the first few weeks of a mouse pup's life affected the number of copies of the L1 retrotransposon. The experience of maternal care was thus “recorded” in the DNA of these mice pups during a time when the brain was still actively developing. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6382" page="1395" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aah3378">1395</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6382" page="1330" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aat3977">1330</jats:related-article> </jats:p>

<jats:title>Keeping the channels open</jats:title> <jats:p> When the rice blast fungus enters a rice cell, the plasma membrane stays intact, so the rice cell remains viable. The fungus then moves to adjacent cells via plasmodesmata, the plant's intercellular channels. Sakulkoo <jats:italic>et al.</jats:italic> used a chemical genetic approach to selectively inhibit a single MAP (mitogen-activated protein) kinase, Pmk1, in the blast fungus. Inhibition of Pmk1 trapped the fungus within a rice cell. Pmk1 regulated the expression of a suite of effector genes involved in suppression of host immunity, allowing the fungus to manipulate plasmodesmal conductance. At the same time, Pmk1 regulated the fungus's hyphal constriction, which allows movement into new host cells. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6382" page="1399" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aaq0892">1399</jats:related-article> </jats:p>

<jats:title>An alternate route for metastatic cells</jats:title> <jats:p> Metastatic tumor cells are thought to reach distant organs by traveling through the blood circulation or the lymphatic system. Two studies of mouse models now suggest a hybrid route for tumor cell dissemination. Pereira <jats:italic>et al.</jats:italic> and Brown <jats:italic>et al.</jats:italic> used distinct methodologies to monitor the fate of tumor cells in lymph nodes. They found that tumor cells could invade local blood vessels within a node, exit the node by entering the blood circulation, then go on to colonize the lung. Whether this dissemination route occurs in cancer patients is unknown; the answer could potentially change the way that affected lymph nodes are treated in cancer. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6382" page="1403" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aal3622">1403</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6382" page="1408" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aal3662">1408</jats:related-article> </jats:p>

<jats:title>An alternate route for metastatic cells</jats:title> <jats:p> Metastatic tumor cells are thought to reach distant organs by traveling through the blood circulation or the lymphatic system. Two studies of mouse models now suggest a hybrid route for tumor cell dissemination. Pereira <jats:italic>et al.</jats:italic> and Brown <jats:italic>et al.</jats:italic> used distinct methodologies to monitor the fate of tumor cells in lymph nodes. They found that tumor cells could invade local blood vessels within a node, exit the node by entering the blood circulation, then go on to colonize the lung. Whether this dissemination route occurs in cancer patients is unknown; the answer could potentially change the way that affected lymph nodes are treated in cancer. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6382" page="1403" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aal3622">1403</jats:related-article> , p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6382" page="1408" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aal3662">1408</jats:related-article> </jats:p>

<jats:title>Using iron to generate a copper ligand</jats:title><jats:p>Many microbial enzymes are metal-dependent, and the microbe must acquire scarce metals from the environment. Microbes that use methane as a carbon source have a copper-dependent enzyme that oxidizes the methane. Peptides known as methanobactins (Mbns) acquire copper by using a pair of ligands comprising a nitrogen-containing ring and an adjacent thioamide. Kenney<jats:italic>et al.</jats:italic>describe the biosynthetic machinery that adds the copper-binding groups to a precursor peptide. This involves a complex of two homologs: MbnB, a member of a functionally uncharacterized protein family that includes a diiron cluster, and MbnC, which is even less well characterized. The iron cofactor is required for ligand synthesis. MbnB and MbnC homologs are encoded in many genomes, suggesting that they may have roles beyond Mbn biosynthesis.</jats:p><jats:p><jats:italic>Science</jats:italic>, this issue p.<jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6382" page="1411" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aap9437">1411</jats:related-article></jats:p>

<jats:title>Local control of localized protein synthesis</jats:title> <jats:p> Localized protein synthesis provides spatiotemporal precision for injury responses and growth decisions at remote positions in nerve axons. Terenzio <jats:italic>et al.</jats:italic> show that this process is controlled by local translation of preexisting axonal mRNA encoding the master regulator mTOR (see the Perspective by Riccio). mTOR controls both its own synthesis and that of most newly synthesized proteins at axonal injury sites, thereby determining the subsequent survival and growth of the injured neuron. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6382" page="1416" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aan1053">1416</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6382" page="1331" related-article-type="in-this-issue" vol="359" xlink:href="10.1126/science.aat1498">1331</jats:related-article> </jats:p>

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