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Institución detectada Período Navegá Descargá Solicitá
No detectada desde mar. 1997 / hasta dic. 2023 Science Journals

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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

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Cobertura temática

Tabla de contenidos

To explain away dark matter, gravity would have to be really weird, cosmologists say

Adrian Cho

Palabras clave: Multidisciplinary.

Pp. No disponible

Response to Comment on “Ancient origins of allosteric activation in a Ser-Thr kinase”

Christopher WilsonORCID; Dorothee KernORCID

<jats:p> Park <jats:italic>et al</jats:italic> . question one out of seven findings from Hadzipasic <jats:italic>et al</jats:italic> .: whether TPX2 allosterically regulates the oldest Aurora. We had already addressed the two concerns raised—sparse sequence sampling and not forcing the gene to the species tree—before publication. Moreover, we believe their ancestral sequence reconstruction would be consistent with a nonallosteric common ancestor, and we show large sequence differences caused by species tree–enforced gene trees. </jats:p>

Palabras clave: Multidisciplinary.

Pp. No disponible

Architecture of the photosynthetic complex from a green sulfur bacterium

Jing-Hua ChenORCID; Hangjun Wu; Caihuang XuORCID; Xiao-Chi Liu; Zihui Huang; Shenghai ChangORCID; Wenda WangORCID; Guangye HanORCID; Tingyun KuangORCID; Jian-Ren ShenORCID; Xing ZhangORCID

<jats:title>Green to the core</jats:title> <jats:p> Light from the Sun powers most life on today's Earth in some way. The core of the photosynthetic apparatus where charge separation occurs, the reaction center (RC), is thought to have originated a single time and diverged, yielding new kinds of complexes adapted to different tasks and environments. Chen <jats:italic>et al.</jats:italic> now present an important missing puzzle piece in our understanding of the evolution of RCs: a cryo–electron microscopy structure of the homodimeric type I RC from a green sulfur bacterium bound to a light-harvesting protein. The observed cofactor and pigment arrangement explain biochemical features of this RC and will aid in our understanding of how a single ancestral RC gave rise to the range of structures and functions seen in RCs today. </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.abb6350">eabb6350</jats:related-article> </jats:p>

Palabras clave: Multidisciplinary.

Pp. No disponible

Autosomal dominant VCP hypomorph mutation impairs disaggregation of PHF-tau

Nabil F. DarwichORCID; Jessica M. PhanORCID; Boram KimORCID; EunRan Suh; John D. PapatriantafyllouORCID; Lakshmi ChangolkarORCID; Aivi T. NguyenORCID; Caroline M. O’Rourke; Zhuohao HeORCID; Sílvia PortaORCID; Garrett S. GibbonsORCID; Kelvin C. LukORCID; Sokratis G. PapageorgiouORCID; Murray GrossmanORCID; Lauren MassimoORCID; David J. IrwinORCID; Corey T. McMillan; Ilya M. NasrallahORCID; Camilo Toro; Geoffrey K. AguirreORCID; Vivianna M. Van Deerlin; Edward B. LeeORCID

<jats:title>Two ways to get tangled?</jats:title> <jats:p> Neurodegeneration in Alzheimer's disease dementia is associated with neurofibrillary tangles composed of aggregated tau protein. Darwich <jats:italic>et al.</jats:italic> describe an additional form of autosomal-dominant dementia with neurofibrillary tangles linked to a hypomorph mutation in valosin-containing protein (VCP). VCP was found to disaggregate pathologic tau, and the hypomorph mutation increased tau accumulation in cells and mice. These findings highlight the role of protein turnover in maintaining neuronal health and suggest that VCP may provide a therapeutic target for Alzheimer's disease. </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.aay8826">eaay8826</jats:related-article> </jats:p>

Palabras clave: Multidisciplinary.

Pp. No disponible

Divergent impacts of warming weather on wildlife disease risk across climates

Jeremy M. CohenORCID; Erin L. SauerORCID; Olivia SantiagoORCID; Samuel SpencerORCID; Jason R. Rohr

<jats:title>Climate change alters disease risks</jats:title> <jats:p> Climate change appears to be provoking changes in the patterns and intensity of infectious diseases. For example, when conditions are cool, amphibians from warm climates experience greater burdens of infection by chytrid fungus than hosts from cool regions. Cohen <jats:italic>et al.</jats:italic> undertook a global metanalysis of 383 studies to test whether this “thermal mismatch” hypothesis holds true over the gamut of host-pathogen relationships. The authors combined date and location data with a selection of host and parasite traits and weather data. In the resulting model, fungal disease risk increased sharply under cold abnormalities in warm climates, whereas bacterial disease prevalence increased sharply under warm abnormalities in cool climates. Warming is projected to benefit helminths more than other parasites, and viral infections showed less obvious relationships with climate change. </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.abb1702">eabb1702</jats:related-article> </jats:p>

Palabras clave: Multidisciplinary.

Pp. No disponible

Comment on “Ancient origins of allosteric activation in a Ser-Thr kinase”

Yeonwoo ParkORCID; Jaeda E. J. PattonORCID; Georg K. A. HochbergORCID; Joseph W. ThorntonORCID

<jats:p> Hadzipasic <jats:italic>et al</jats:italic> . (Reports, 21 February 2020, p. 912) used ancestral sequence reconstruction to identify historical sequence substitutions that putatively caused Aurora kinases to evolve allosteric regulation. We show that their results arise from using an implausible phylogeny and sparse sequence sampling. Addressing either problem reverses their inferences: Allostery and the amino acids that confer it were not gained during the diversification of eukaryotes but were lost in a subgroup of Fungi. </jats:p>

Palabras clave: Multidisciplinary.

Pp. No disponible

Rotavirus induces intercellular calcium waves through ADP signaling

Alexandra L. Chang-GrahamORCID; Jacob L. PerryORCID; Melinda A. EngevikORCID; Kristen A. EngevikORCID; Francesca J. ScribanoORCID; J. Thomas GebertORCID; Heather A. DanhofORCID; Joel C. NelsonORCID; Joseph S. Kellen; Alicia C. Strtak; Narayan P. SastriORCID; Mary K. EstesORCID; Robert A. BrittonORCID; James Versalovic; Joseph M. HyserORCID

<jats:title>Riding the calcium waves</jats:title> <jats:p> Rotavirus causes severe diarrhea and vomiting in children worldwide, yet how infection causes these diseases remains poorly understood. A leading theory is that virus-infected cells secrete paracrine signaling molecules that dysregulate epithelial cells. Chang-Graham <jats:italic>et al.</jats:italic> found that rotavirus-infected cells trigger cell-to-cell signaling that manifests as intercellular calcium waves (see the Perspective by Stanifer and Boulant). This signal results from the repeated release of adenosine 5′-diphosphate by rotavirus-infected cells. This release activates receptors on nearby uninfected cells, resulting in a calcium signal. The intercellular calcium waves activate chloride and serotonin secretion, which contributes to diarrhea and vomiting. Blocking this paracrine signal could represent a target for antidiarrheal pharmacotherapy. </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.abc3621">eabc3621</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6519" page="909" related-article-type="in-this-issue" vol="370" xlink:href="10.1126/science.abf1914">909</jats:related-article> </jats:p>

Palabras clave: Multidisciplinary.

Pp. No disponible

Gene regulatory networks controlling vertebrate retinal regeneration

Thanh HoangORCID; Jie WangORCID; Patrick BoydORCID; Fang WangORCID; Clayton SantiagoORCID; Lizhi Jiang; Sooyeon YooORCID; Manuela LahneORCID; Levi J. ToddORCID; Meng JiaORCID; Cristian SaezORCID; Casey KeuthanORCID; Isabella PalazzoORCID; Natalie SquiresORCID; Warren A. CampbellORCID; Fatemeh RajaiiORCID; Trisha ParayilORCID; Vickie TrinhORCID; Dong Won Kim; Guohua WangORCID; Leah J. CampbellORCID; John AshORCID; Andy J. FischerORCID; David R. HydeORCID; Jiang QianORCID; Seth BlackshawORCID

<jats:title>Unlocking retinal regeneration in mice</jats:title> <jats:p> Zebrafish can regenerate damaged retinal tissue, but mice cannot. Hoang <jats:italic>et al.</jats:italic> found that tracking changes in gene expression and chromatin accessibility upon injury revealed clues as to why retinal glial cells in zebrafish could generate new neurons but the same cell type in mice could not. In zebrafish, activated Müller glial cells shift into a proliferative phase, whereas in mice, a genetic network returns the glial cells to quiescence. A few transcription factors enforce quiescence in the mouse, and disruption of these allowed Müller glia to proliferate and generate new neurons after retinal injury. </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.abb8598">eabb8598</jats:related-article> </jats:p>

Palabras clave: Multidisciplinary.

Pp. No disponible

Fire and biodiversity in the Anthropocene

Luke T. KellyORCID; Katherine M. GiljohannORCID; Andrea DuaneORCID; Núria AquiluéORCID; Sally ArchibaldORCID; Enric BatlloriORCID; Andrew F. BennettORCID; Stephen T. Buckland; Quim CanellesORCID; Michael F. ClarkeORCID; Marie-Josée FortinORCID; Virgilio HermosoORCID; Sergi HerrandoORCID; Robert E. KeaneORCID; Frank K. Lake; Michael A. McCarthyORCID; Alejandra Morán-OrdóñezORCID; Catherine L. ParrORCID; Juli G. PausasORCID; Trent D. PenmanORCID; Adrián RegosORCID; Libby RumpffORCID; Julianna L. SantosORCID; Annabel L. SmithORCID; Alexandra D. SyphardORCID; Morgan W. TingleyORCID; Lluís BrotonsORCID

<jats:p>Fire has been a source of global biodiversity for millions of years. However, interactions with anthropogenic drivers such as climate change, land use, and invasive species are changing the nature of fire activity and its impacts. We review how such changes are threatening species with extinction and transforming terrestrial ecosystems. Conservation of Earth’s biological diversity will be achieved only by recognizing and responding to the critical role of fire. In the Anthropocene, this requires that conservation planning explicitly includes the combined effects of human activities and fire regimes. Improved forecasts for biodiversity must also integrate the connections among people, fire, and ecosystems. Such integration provides an opportunity for new actions that could revolutionize how society sustains biodiversity in a time of changing fire activity.</jats:p>

Palabras clave: Multidisciplinary.

Pp. eabb0355

The excellence question

Ottoline Leyser

<jats:p>Five months ago, when I stepped into my new role as the chief executive officer of the UK Research and Innovation (UKRI) organization, a question loomed large for me: What is excellence? After all, UKRI is the major public funder of science in the United Kingdom, spending billions of taxpayer money every year. To spend this money well, UKRI must support a portfolio of truly excellent work. So, what then is excellence?</jats:p>

Palabras clave: Multidisciplinary.

Pp. 886-886