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Science
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Disponibilidad
| Institución detectada | Período | Navegá | Descargá | Solicitá |
|---|---|---|---|---|
| No detectada | desde mar. 1997 / hasta dic. 2023 | Science Journals |
Información
Tipo de recurso:
revistas
ISSN impreso
0036-8075
ISSN electrónico
1095-9203
Editor responsable
American Association for the Advancement of Science (AAAS)
País de edición
Estados Unidos
Fecha de publicación
1880-
Cobertura temática
Tabla de contenidos
Response to Comment on “Forest microclimate dynamics drive plant responses to warming”
Florian Zellweger
; Pieter De Frenne
; Jonathan Lenoir
; Pieter Vangansbeke
; Kris Verheyen
; Markus Bernhardt-Römermann
; Lander Baeten
; Radim Hédl
; Imre Berki
; Jörg Brunet
; Hans Van Calster
; Markéta Chudomelová
; Guillaume Decocq; Thomas Dirnböck
; Tomasz Durak
; Thilo Heinken
; Bogdan Jaroszewicz
; Martin Kopecký
; František Máliš
; Martin Macek
; Marek Malicki
; Tobias Naaf
; Thomas A. Nagel
; Adrienne Ortmann-Ajkai
; Petr Petřík
; Remigiusz Pielech
; Kamila Reczyńska
; Wolfgang Schmidt
; Tibor Standovár
; Krzysztof Świerkosz
; Balázs Teleki; Ondřej Vild
; Monika Wulf
; David Coomes
<jats:p> Bertrand <jats:italic>et al</jats:italic> . question our interpretation about warming effects on the thermophilization in forest plant communities and propose an alternative way to analyze climatic debt. We show that microclimate warming is a better predictor than macroclimate warming for studying forest plant community responses to warming. Their additional analyses do not affect or change our interpretations and conclusions. </jats:p>
Palabras clave: Multidisciplinary.
Pp. No disponible
Protein storytelling through physics
Emiliano Brini
; Carlos Simmerling
; Ken Dill
<jats:title>Understanding what drives proteins</jats:title> <jats:p> Computational molecular physics (CMP) aims to leverage the laws of physics to understand not just static structures but also the motions and actions of biomolecules. Applying CMP to proteins has required either simplifying the physical models or running simulations that are shorter than the time scale of the biological activity. Brini <jats:italic>et al.</jats:italic> reviewed advances that are moving CMP to time scales that match biological events such as protein folding, ligand unbinding, and some conformational changes. They also highlight the role of blind competitions in driving the field forward. New methods such as deep learning approaches are likely to make CMP an increasingly powerful tool in describing proteins in action. </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.aaz3041">eaaz3041</jats:related-article> </jats:p>
Palabras clave: Multidisciplinary.
Pp. No disponible
In vivo Perturb-Seq reveals neuronal and glial abnormalities associated with autism risk genes
Xin Jin
; Sean K. Simmons; Amy Guo; Ashwin S. Shetty
; Michelle Ko; Lan Nguyen; Vahbiz Jokhi; Elise Robinson; Paul Oyler
; Nathan Curry; Giulio Deangeli; Simona Lodato
; Joshua Z. Levin
; Aviv Regev
; Feng Zhang
; Paola Arlotta
<jats:title>An in vivo analysis of autism risk genes</jats:title> <jats:p> CRISPR targeting in vivo, especially in mammals, can be difficult and time consuming when attempting to determine the effects of a single gene. However, such studies may be required to identify pathological gene variants with effects in specific cells along a developmental trajectory. To study the function of genes implicated in autism spectrum disorders (ASDs), Jin <jats:italic>et al.</jats:italic> applied a gene-editing and single-cell–sequencing system, Perturb-Seq, to knock out 35 ASD candidate genes in multiple mice embryos (see the Perspective by Treutlein and Camp). This method identified networks of gene expression in neuronal and glial cells that suggest new functions in ASD-related genes. </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.aaz6063">eaaz6063</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6520" page="1038" related-article-type="in-this-issue" vol="370" xlink:href="10.1126/science.abf3661">1038</jats:related-article> </jats:p>
Palabras clave: Multidisciplinary.
Pp. No disponible
Identification of Integrator-PP2A complex (INTAC), an RNA polymerase II phosphatase
Hai Zheng
; Yilun Qi
; Shibin Hu
; Xuan Cao
; Congling Xu
; Zhinang Yin
; Xizi Chen
; Yan Li
; Weida Liu
; Jie Li; Jiawei Wang
; Gang Wei
; Kaiwei Liang
; Fei Xavier Chen
; Yanhui Xu
<jats:title>Dephosphorylating RNA polymerase II</jats:title> <jats:p> Transcription in metazoans requires coordination of multiple factors to control the progression of polymerases and the integrity of their RNA products. Zheng <jats:italic>et al.</jats:italic> identified a new dual-enzyme complex called INTAC, which is composed of protein phosphatase 2A (PP2A) core enzyme and the multisubunit RNA endonuclease Integrator. Structural and functional studies show that INTAC functions as a noncanonical PP2A holoenzyme that dephosphorylates the C-terminal domain of RNA polymerase II to attenuate transcription. This study provides a direct connection between PP2A-mediated dephosphorylation and transcriptional regulation, two fundamental cellular processes. </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.abb5872">eabb5872</jats:related-article> </jats:p>
Palabras clave: Multidisciplinary.
Pp. No disponible
Abl and Canoe/Afadin mediate mechanotransduction at tricellular junctions
Huapeng H. Yu
; Jennifer A. Zallen
<jats:title>Tension where multiple cells meet</jats:title> <jats:p> Cells exist in varying environments and must respond to specific stimuli. During development, epithelial cells need to rapidly reorganize under tension without compromising epithelial integrity. Yu <jats:italic>et al.</jats:italic> demonstrate that <jats:italic>Drosophila</jats:italic> epithelial cells achieve this by transiently stabilizing adhesion at tricellular junctions where three cells meet (see the Perspective by Raghavan and Vasioukhin). The conserved adhesion regulator Canoe/Afadin is recruited to tricellular junctions under tension within seconds and dissociates when tension is released through a mechanism that requires Abl-dependent tyrosine phosphorylation. These results identify an in vivo mechanotransduction pathway that dynamically couples tricellular adhesion with physiological forces, allowing cells to rapidly modulate their behavior in response to mechanical changes in their environment. </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.aba5528">eaba5528</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6520" page="1036" related-article-type="in-this-issue" vol="370" xlink:href="10.1126/science.abf2782">1036</jats:related-article> </jats:p>
Palabras clave: Multidisciplinary.
Pp. No disponible
Viral epitope profiling of COVID-19 patients reveals cross-reactivity and correlates of severity
Ellen Shrock
; Eric Fujimura
; Tomasz Kula
; Richard T. Timms
; I-Hsiu Lee
; Yumei Leng
; Matthew L. Robinson
; Brandon M. Sie
; Mamie Z. Li
; Yuezhou Chen; Jennifer Logue; Adam Zuiani
; Denise McCulloch
; Felipe J. N. Lelis
; Stephanie Henson; Daniel R. Monaco; Meghan Travers
; Shaghayegh Habibi
; William A. Clarke; Patrizio Caturegli; Oliver Laeyendecker; Alicja Piechocka-Trocha
; Jonathan Z. Li
; Ashok Khatri
; Helen Y. Chu; Alexandra-Chloé Villani
; Kyle Kays; Marcia B. Goldberg
; Nir Hacohen
; Michael R. Filbin
; Xu G. Yu
; Bruce D. Walker
; Duane R. Wesemann
; H. Benjamin Larman; James A. Lederer; Stephen J. Elledge
; Kendall Lavin-Parsons; Blair Parry; Brendan Lilley; Carl Lodenstein; Brenna McKaig; Nicole Charland; Hargun Khanna; Justin Margolin; Anna Gonye; Irena Gushterova; Tom Lasalle; Nihaarika Sharma; Brian C. Russo; Maricarmen Rojas-Lopez; Moshe Sade-Feldman; Kasidet Manakongtreecheep; Jessica Tantivit; Molly Fisher Thomas; Betelihem A. Abayneh; Patrick Allen; Diane Antille; Katrina Armstrong; Siobhan Boyce; Joan Braley; Karen Branch; Katherine Broderick; Julia Carney; Andrew Chan; Susan Davidson; Michael Dougan; David Drew; Ashley Elliman; Keith Flaherty; Jeanne Flannery; Pamela Forde; Elise Gettings; Amanda Griffin; Sheila Grimmel; Kathleen Grinke; Kathryn Hall; Meg Healy; Deborah Henault; Grace Holland; Chantal Kayitesi; Vlasta LaValle; Yuting Lu; Sarah Luthern; Jordan Marchewka (Schneider); Brittani Martino; Roseann McNamara; Christian Nambu; Susan Nelson; Marjorie Noone; Christine Ommerborn; Lois Chris Pacheco; Nicole Phan; Falisha A. Porto; Edward Ryan; Kathleen Selleck; Sue Slaughenhaupt; Kimberly Smith Sheppard; Elizabeth Suschana; Vivine Wilson; Galit Alter; Alejandro Balazs; Julia Bals; Max Barbash; Yannic Bartsch; Julie Boucau; Josh Chevalier; Fatema Chowdhury; Kevin Einkauf; Jon Fallon; Liz Fedirko; Kelsey Finn; Pilar Garcia-Broncano; Ciputra Hartana; Chenyang Jiang; Paulina Kaplonek; Marshall Karpell; Evan C. Lam; Kristina Lefteri; Xiaodong Lian; Mathias Lichterfeld; Daniel Lingwood; Hang Liu; Jinqing Liu; Natasha Ly; Ashlin Michell; Ilan Millstrom; Noah Miranda; Claire O’Callaghan; Matthew Osborn; Shiv Pillai; Yelizaveta Rassadkina; Alexandra Reissis; Francis Ruzicka; Kyra Seiger; Libera Sessa; Christianne Sharr; Sally Shin; Nishant Singh; Weiwei Sun; Xiaoming Sun; Hannah Ticheli; Alicja Trocha-Piechocka; Daniel Worrall; Alex Zhu; George Daley; David Golan; Howard Heller; Arlene Sharpe; Nikolaus Jilg; Alex Rosenthal; Colline Wong;
<jats:title>Profiling coronaviruses</jats:title> <jats:p> Among the coronaviruses that infect humans, four cause mild common colds, whereas three others, including the currently circulating severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), result in severe infections. Shrock <jats:italic>et al.</jats:italic> used a technology known as VirScan to probe the antibody repertoires of hundreds of coronavirus disease 2019 (COVID-19) patients and pre–COVID-19 era controls. They identified hundreds of antibody targets, including several antibody epitopes shared by the mild and severe coronaviruses and many specific to SARS-CoV-2. A machine-learning model accurately classified patients infected with SARS-CoV-2 and guided the design of an assay for rapid SARS-CoV-2 antibody detection. The study also looked at how the antibody response and viral exposure history differ in patients with diverging outcomes, which could inform the production of improved vaccine and antibody therapies. </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.abd4250">eabd4250</jats:related-article> </jats:p>
Palabras clave: Multidisciplinary.
Pp. No disponible
Comment on “Forest microclimate dynamics drive plant responses to warming”
Romain Bertrand
; Fabien Aubret; Gaël Grenouillet
; Alexandre Ribéron; Simon Blanchet
<jats:p> Zellweger <jats:italic>et al</jats:italic> . (Reports, 15 May 2020, p. 772) claimed that forest plant communities’ response to global warming is primarily controlled by microclimate dynamics. We show that community thermophilization is poorly explained by the underlying components of microclimate, and that global warming primarily controls the climatic lag of plant communities. Deconstructing the underlying components of microclimate provides insights for managers. </jats:p>
Palabras clave: Multidisciplinary.
Pp. No disponible
Modeling, post COVID-19
William H. Press; Richard C. Levin
<jats:p>Much of the public first learned about epidemiological modeling during the early months of the coronavirus disease 2019 (COVID-19) pandemic. The first models resulted in more confusion than clarity. Even though coronavirus cases were rising exponentially in the United States and Europe, some models predicted a rapid peak followed by a rapid decline, whereas other models predicted cycles of infection continuing over several years. Much has been learned since those early months. In retrospect, it is clear that modeling requires both reliable data and an accurate understanding of how disease spreads, and that the field of epidemiological modeling requires a diversity of approaches. Support for this field must increase and be coordinated, with a designation of responsibilities among funding agencies.</jats:p>
Palabras clave: Multidisciplinary.
Pp. 1015-1015
News at a glance
<jats:p>A roundup of weekly science policy and related news.</jats:p>
Palabras clave: Multidisciplinary.
Pp. 1016-1017
Arecibo radio telescope to be decommissioned
Daniel Clery
<jats:p>Famed observatory set for demolition after cable failures put it on the brink of collapse.</jats:p>
Palabras clave: Multidisciplinary.
Pp. 1018-1019