Catálogo de publicaciones - revistas

<jats:title>Signals of Mosquito Speciation</jats:title> <jats:p> Malaria in Africa is transmitted by the mosquito species complex <jats:italic>Anopheles gambiae</jats:italic> . <jats:bold> Neafsey <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="514" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1193036">514</jats:related-article> ) made high-resolution single-nucleotide arrays to map genetic divergence among members of the species. Differentiation between populations was observed and evidence obtained for selective sweeps within populations. Most divergence occurred within inversion regions around the centrosome and in genes associated with development, pheromone signaling, and from the X chromosome. The analysis also revealed signals of sympatric speciation occurring within similar chromosomal regions in mosquitoes from different regions in Africa. <jats:bold> Lawniczak <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="512" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1195755">512</jats:related-article> ) sequenced the genomes of two molecular forms (known as M and S) of <jats:italic>A. gambiae</jats:italic> , which have distinctive behavioral phenotypes and appear to be speciating. This effort resolves problems arising from the apparently chimeric nature of the reference genome and confirms the observed genome-wide divergences. This kind of analysis has the potential to contribute to control programs that can adapt to population shifts in mosquito behavior arising from the selective effects of the control measures themselves. </jats:p>

<jats:title>Signals of Mosquito Speciation</jats:title> <jats:p> Malaria in Africa is transmitted by the mosquito species complex <jats:italic>Anopheles gambiae</jats:italic> . <jats:bold> Neafsey <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="514" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1193036">514</jats:related-article> ) made high-resolution single-nucleotide arrays to map genetic divergence among members of the species. Differentiation between populations was observed and evidence obtained for selective sweeps within populations. Most divergence occurred within inversion regions around the centrosome and in genes associated with development, pheromone signaling, and from the X chromosome. The analysis also revealed signals of sympatric speciation occurring within similar chromosomal regions in mosquitoes from different regions in Africa. <jats:bold> Lawniczak <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="512" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1195755">512</jats:related-article> ) sequenced the genomes of two molecular forms (known as M and S) of <jats:italic>A. gambiae</jats:italic> , which have distinctive behavioral phenotypes and appear to be speciating. This effort resolves problems arising from the apparently chimeric nature of the reference genome and confirms the observed genome-wide divergences. This kind of analysis has the potential to contribute to control programs that can adapt to population shifts in mosquito behavior arising from the selective effects of the control measures themselves. </jats:p>

<jats:title>Stress, DNA Damage, and ATM</jats:title> <jats:p> The protein kinase ATM (ataxia-telangiectasia mutated) is a key component of the signaling pathway through which cells are protected from DNA damage. ATM becomes activated within a protein complex at sites of double-stranded breaks in DNA. ATM is also activated in response to increased production of reactive oxygen species (ROS). Such activation was thought to reflect DNA damage caused by ROS, but <jats:bold> Guo <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="517" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1192912">517</jats:related-article> ) showed that ATM was in fact directly activated by ROS. A cysteine residue in ATM contributes to the formation of disulfide-linked dimers of activated ATM on exposure to ROS in vitro. Experiments using mutated forms of the enzyme suggested that two distinct mechanisms regulated ATM activity. </jats:p>

<jats:title>PIAS1 Repression</jats:title> <jats:p> Regulatory T cells (T <jats:sub>regs</jats:sub> ) promote immune tolerance and protect against autoimmunity. T <jats:sub>regs</jats:sub> develop in the thymus, and their differentiation and acquisition of suppressive function requires expression of the transcription factor Foxp3. Although several transcription factors have been identified that turn on <jats:italic>Foxp3</jats:italic> gene expression, how Foxp3 remains turned off in non-T <jats:sub>regs</jats:sub> is not well understood. <jats:bold> Liu <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="521" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1193787">521</jats:related-article> ) have demonstrated that a regulator of cytokine signaling, PIAS1, represses Foxp3 expression by chromatin modification. PIAS1 promoted the methylation of the <jats:italic>Foxp3</jats:italic> promoter by recruiting methyltransferases to inhibit expression. PIAS-deficient mice have more T <jats:sub>reg</jats:sub> cells than controls, and they appear to be protected against the development of experimental autoimmune encephalomyelitis, a mouse model for multiple sclerosis. </jats:p>

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