Catálogo de publicaciones - revistas

<jats:title>From development to disease</jats:title> <jats:p> When brain development goes awry, whether in genes or cells or circuits, neurodevelopmental disorders ensue. Klingler <jats:italic>et al.</jats:italic> review how disrupted development leads to clinical symptoms, with a particular focus on the linkage between cortical malformations and neuropsychiatric disorders. The complexity of the developmental process may underlie the variability in symptoms. </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" related-article-type="in-this-issue" xlink:href="10.1126/science.aba4517">eaba4517</jats:related-article> </jats:p>

<jats:title>Cellular beauty is skin deep</jats:title> <jats:p> Human skin works as barrier, preventing the entry of pathogens, among other functions. Reynolds <jats:italic>et al.</jats:italic> used single-cell sequencing to generate an atlas of the human skin from both developing and adult sources, identifying differences and similarities across heterogeneous populations of skin cells. In this atlas, gene expression in the two disease states studied—atopic dermatitis and psoriasis—varied from that in a healthy adult, suggesting that a fetal skin signature is expressed in adult inflamed skin. Furthermore, differences in immune cell composition between healthy fetal and adult skin and that of individuals suffering from disease were observed. </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" related-article-type="in-this-issue" xlink:href="10.1126/science.aba6500">eaba6500</jats:related-article> </jats:p>

<jats:title>Cross-talk between histone modifications</jats:title> <jats:p> Histone modifications play pivotal roles within the intricate protein networks that underlie transcription and gene silencing in eukaryotic genomes. The enzymes that deposit them undergo spatiotemporal fine-tuning of their catalytic activity; one example is trans-histone cross-talk, in which one histone modification activates an enzyme responsible for another histone modification. Valencia-Sánchez <jats:italic>et al.</jats:italic> show that histone H4 lysine 16 acetylation (H4K16ac), a hallmark of decondensed, transcriptionally permissive chromatin, directly stimulates the Dot1 histone H3 lysine 79 methyltransferase. Structural, biochemical, and cellular data explain Dot1's regulation by H4K16ac and show how it coordinates with a second positive regulator of Dot1, histone H2B ubiquitination. </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" related-article-type="in-this-issue" xlink:href="10.1126/science.abc6663">eabc6663</jats:related-article> </jats:p>

<jats:title>Cryo-EM uncovers polycomb interactions</jats:title> <jats:p> Polycomb family enzymes include the chromatin modifiers PRC1 and PRC2, which are involved in gene repression. Although the catalytic functions of these complexes are well known, their functional relationship is not. Kasinath <jats:italic>et al.</jats:italic> used cryo–electron microscopy (cryo-EM) to visualize the interactions between nucleosomes containing ubiquitinated histone H2A, the product of PRC1, and the PRC2-activating cofactors JARID2 and AEBP2, providing the molecular basis for PRC1-dependent recruitment of PRC2. They also show that JARID2 and AEBP2 partially overcome the inhibitory effect of PRC2 by two trimethyl lysine transcription marks on histones. This work suggests that PRC2 regulation involves an intricate interplay between PRC2 cofactors and histone posttranslational modifications. </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" related-article-type="in-this-issue" xlink:href="10.1126/science.abc3393">eabc3393</jats:related-article> </jats:p>

<jats:p>Mental health and well-being are critical to student success in higher education and beyond but rarely get the attention they need. Colleges and universities in the United States have been seeing increases in mental illness and emotional distress among students for decades. Unfortunately, the COVID-19 pandemic and its social and economic consequences are accelerating these trends. Furthermore, renewed focus on systemic racism in many spheres of American life is highlighting the stresses and mental health consequences faced by students from traditionally underrepresented groups and by women who continue to suffer the lingering effects of sexism. The damaging consequences of these problems for students, their institutions, and a modern world that depends on a well-educated, healthy workforce demand a much better response. Promoting student mental health and emotional well-being on campus requires more than a well-functioning counseling center. It calls for a campus-wide commitment and coordinated action plan. For many institutions, accomplishing this will involve a major rethinking of their responsibilities to students.</jats:p>

<jats:p>A roundup of weekly science policy and related news.</jats:p>

<jats:p>SARS-CoV-2 variants found in Brazil and South Africa may evade human antibodies.</jats:p>

<jats:p>Journal mentions of studies based on disputed data from Surgisphere often fail to clearly flag retractions.</jats:p>