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Quantifying the drivers and predictability of seasonal changes in African fire 期刊论文
NATURE COMMUNICATIONS, 2020, 11 (1)
作者:  Yu, Yan;  Mao, Jiafu;  Thornton, Peter E.;  Notaro, Michael;  Wullschleger, Stan D.;  Shi, Xiaoying;  Hoffman, Forrest M.;  Wang, Yaoping
收藏  |  浏览/下载:9/0  |  提交时间:2020/06/16
Synthesis and properties of free-standing monolayer amorphous carbon 期刊论文
NATURE, 2020, 577 (7789) : 199-+
作者:  Toh, Chee-Tat;  Zhang, Hongji;  Lin, Junhao;  Mayorov, Alexander S.;  Wang, Yun-Peng;  Orofeo, Carlo M.;  Ferry, Darim Badur;  Andersen, Henrik;  Kakenov, Nurbek;  Guo, Zenglong;  Abidi, Irfan Haider;  Sims, Hunter;  Suenaga, Kazu;  Pantelides, Sokrates T.;  Ozyilmaz, Barbaros
收藏  |  浏览/下载:7/0  |  提交时间:2020/07/03

Bulk amorphous materials have been studied extensively and are widely used, yet their atomic arrangement remains an open issue. Although they are generally believed to be Zachariasen continuous random networks(1), recent experimental evidence favours the competing crystallite model in the case of amorphous silicon(2-4). In two-dimensional materials, however, the corresponding questions remain unanswered. Here we report the synthesis, by laser-assisted chemical vapour deposition(5), of centimetre-scale, free-standing, continuous and stable monolayer amorphous carbon, topologically distinct from disordered graphene. Unlike in bulk materials, the structure of monolayer amorphous carbon can be determined by atomic-resolution imaging. Extensive characterization by Raman and X-ray spectroscopy and transmission electron microscopy reveals the complete absence of long-range periodicity and a threefold-coordinated structure with a wide distribution of bond lengths, bond angles, and five-, six-, seven- and eight-member rings. The ring distribution is not a Zachariasen continuous random network, but resembles the competing (nano)crystallite model(6). We construct a corresponding model that enables density-functional-theory calculations of the properties of monolayer amorphous carbon, in accordance with observations. Direct measurements confirm that it is insulating, with resistivity values similar to those of boron nitride grown by chemical vapour deposition. Free-standing monolayer amorphous carbon is surprisingly stable and deforms to a high breaking strength, without crack propagation from the point of fracture. The excellent physical properties of this stable, free-standing monolayer amorphous carbon could prove useful for permeation and diffusion barriers in applications such as magnetic recording devices and flexible electronics.


  
Decreased motility of flagellated microalgae long-term acclimated to CO2-induced acidified waters 期刊论文
NATURE CLIMATE CHANGE, 2020, 10 (6) : 561-+
作者:  Wang, Yitao;  Fan, Xiao;  Gao, Guang;  Beardall, John;  Inaba, Kazuo;  Hall-Spencer, Jason M.;  Xu, Dong;  Zhang, Xiaowen;  Han, Wentao;  McMinn, Andrew;  Ye, Naihao
收藏  |  浏览/下载:13/0  |  提交时间:2020/06/09
Bedrock geochemistry influences vegetation growth by regulating the regolith water holding capacity 期刊论文
NATURE COMMUNICATIONS, 2020, 11 (1)
作者:  Jiang, Zihan;  Liu, Hongyan;  Wang, Hongya;  Peng, Jian;  Meersmans, Jeroen;  Green, Sophie M.;  Quine, Timothy A.;  Wu, Xiuchen;  Song, Zhaoliang
收藏  |  浏览/下载:15/0  |  提交时间:2020/05/20
Mutations that prevent caspase cleavage of RIPK1 cause autoinflammatory disease 期刊论文
NATURE, 2020, 577 (7788) : 103-+
作者:  Lalaoui, Najoua;  Boyden, Steven E.;  Oda, Hirotsugu;  Wood, Geryl M.;  Stone, Deborah L.;  Chau, Diep;  Liu, Lin;  Stoffels, Monique;  Kratina, Tobias;  Lawlor, Kate E.;  Zaal, Kristien J. M.;  Hoffmann, Patrycja M.;  Etemadi, Nima;  Shield-Artin, Kristy;  Biben, Christine;  Tsai, Wanxia Li;  Blake, Mary D.;  Kuehn, Hye Sun;  Yang, Dan;  Anderton, Holly;  Silke, Natasha;  Wachsmuth, Laurens;  Zheng, Lixin;  Moura, Natalia Sampaio;  Beck, David B.;  Gutierrez-Cruz, Gustavo;  Ombrello, Amanda K.;  Pinto-Patarroyo, Gineth P.;  Kueh, Andrew J.;  Herold, Marco J.;  Hall, Cathrine;  Wang, Hongying;  Chae, Jae Jin;  Dmitrieva, Natalia I.;  McKenzie, Mark;  Light, Amanda;  Barham, Beverly K.;  Jones, Anne;  Romeo, Tina M.;  Zhou, Qing;  Aksentijevich, Ivona;  Mullikin, James C.;  Gross, Andrew J.;  Shum, Anthony K.;  Hawkins, Edwin D.;  Masters, Seth L.;  Lenardo, Michael J.;  Boehm, Manfred;  Rosenzweig, Sergio D.;  Pasparakis, Manolis;  Voss, Anne K.;  Gadina, Massimo;  Kastner, Daniel L.;  Silke, John
收藏  |  浏览/下载:24/0  |  提交时间:2020/07/03

RIPK1 is a key regulator of innate immune signalling pathways. To ensure an optimal inflammatory response, RIPK1 is regulated post-translationally by well-characterized ubiquitylation and phosphorylation events, as well as by caspase-8-mediated cleavage1-7. The physiological relevance of this cleavage event remains unclear, although it is thought to inhibit activation of RIPK3 and necroptosis8. Here we show that the heterozygous missense mutations D324N, D324H and D324Y prevent caspase cleavage of RIPK1 in humans and result in an early-onset periodic fever syndrome and severe intermittent lymphadenopathy-a condition we term '  cleavage-resistant RIPK1-induced autoinflammatory syndrome'  . To define the mechanism for this disease, we generated a cleavage-resistant Ripk1(D325A) mutant mouse strain. Whereas Ripk1(-/-) mice died postnatally from systemic inflammation, Ripk1(D325A/D325A) mice died during embryogenesis. Embryonic lethality was completely prevented by the combined loss of Casp8 and Ripk3, but not by loss of Ripk3 or Mlkl alone. Loss of RIPK1 kinase activity also prevented Ripk1(D325A/D325A) embryonic lethality, although the mice died before weaning from multi-organ inflammation in a RIPK3-dependent manner. Consistently, Ripk1(D325A/D325A) and Ripk1(D325A/+) cells were hypersensitive to RIPK3-dependent TNF-induced apoptosis and necroptosis. Heterozygous Ripk1(D325A/+) mice were viable and grossly normal, but were hyper-responsive to inflammatory stimuli in vivo. Our results demonstrate the importance of caspase-mediated RIPK1 cleavage during embryonic development and show that caspase cleavage of RIPK1 not only inhibits necroptosis but also maintains inflammatory homeostasis throughout life.


  
A dominant autoinflammatory disease caused by non-cleavable variants of RIPK1 期刊论文
NATURE, 2020, 577 (7788) : 109-+
作者:  Tao, Panfeng;  Sun, Jinqiao;  Wu, Zheming;  Wang, Shihao;  Wang, Jun;  Li, Wanjin;  Pan, Heling;  Bai, Renkui;  Zhang, Jiahui;  Wang, Ying;  Lee, Pui Y.;  Ying, Wenjing;  Zhou, Qinhua;  Hou, Jia;  Wang, Wenjie;  Sun, Bijun;  Yang, Mi;  Liu, Danru;  Fang, Ran;  Han, Huan;  Yang, Zhaohui;  Huang, Xin;  Li, Haibo;  Deuitch, Natalie;  Zhang, Yuan;  Dissanayake, Dilan;  Haude, Katrina;  McWalter, Kirsty;  Roadhouse, Chelsea;  MacKenzie, Jennifer J.;  Laxer, Ronald M.;  Aksentijevich, Ivona;  Yu, Xiaomin;  Wang, Xiaochuan;  Yuan, Junying;  Zhou, Qing
收藏  |  浏览/下载:24/0  |  提交时间:2020/07/03

Activation of RIPK1 controls TNF-mediated apoptosis, necroptosis and inflammatory pathways(1). Cleavage of human and mouse RIPK1 after residues D324 and D325, respectively, by caspase-8 separates the RIPK1 kinase domain from the intermediate and death domains. The D325A mutation in mouse RIPK1 leads to embryonic lethality during mouse development(2,3). However, the functional importance of blocking caspase-8-mediated cleavage of RIPK1 on RIPK1 activation in humans is unknown. Here we identify two families with variants in RIPK1 (D324V and D324H) that lead to distinct symptoms of recurrent fevers and lymphadenopathy in an autosomaldominant manner. Impaired cleavage of RIPK1 D324 variants by caspase-8 sensitized patients'  peripheral blood mononuclear cells to RIPK1 activation, apoptosis and necroptosis induced by TNF. The patients showed strong RIPK1-dependent activation of inflammatory signalling pathways and overproduction of inflammatory cytokines and chemokines compared with unaffected controls. Furthermore, we show that expression of the RIPK1 mutants D325V or D325H in mouse embryonic fibroblasts confers not only increased sensitivity to RIPK1 activation-mediated apoptosis and necroptosis, but also induction of pro-inflammatory cytokines such as IL-6 and TNF. By contrast, patient-derived fibroblasts showed reduced expression of RIPK1 and downregulated production of reactive oxygen species, resulting in resistance to necroptosis and ferroptosis. Together, these data suggest that human non-cleavable RIPK1 variants promote activation of RIPK1, and lead to an autoinflammatory disease characterized by hypersensitivity to apoptosis and necroptosis and increased inflammatory response in peripheral blood mononuclear cells, as well as a compensatory mechanism to protect against several pro-death stimuli in fibroblasts.


  
Global CO2 emissions from dry inland waters share common drivers across ecosystems 期刊论文
NATURE COMMUNICATIONS, 2020, 11 (1)
作者:  Keller, P. S.;  Catalan, N.;  von Schiller, D.;  Grossart, H-P;  Koschorreck, M.;  Obrador, B.;  Frassl, M. A.;  Karakaya, N.;  Barros, N.;  Howitt, J. A.;  Mendoza-Lera, C.;  Pastor, A.;  Flaim, G.;  Aben, R.;  Riis, T.;  Arce, M., I;  Onandia, G.;  Paranaiba, J. R.;  Linkhorst, A.;  del Campo, R.;  Amado, A. M.;  Cauvy-Fraunie, S.;  Brothers, S.;  Condon, J.;  Mendonca, R. F.;  Reverey, F.;  Room, E-, I;  Datry, T.;  Roland, F.;  Laas, A.;  Obertegger, U.;  Park, J-H;  Wang, H.;  Kosten, S.;  Gomez, R.;  Feijoo, C.;  Elosegi, A.;  Sanchez-Montoya, M. M.;  Finlayson, C. M.;  Melita, M.;  Oliveira Junior, E. S.;  Muniz, C. C.;  Gomez-Gener, L.;  Leigh, C.;  Zhang, Q.;  Marce, R.
收藏  |  浏览/下载:14/0  |  提交时间:2020/05/13
Fatty acids and cancer-amplified ZDHHC19 promote STAT3 activation throughS-palmitoylation (vol 573, pg 139, 2019) (Retraction of Vol 573, Pg 139, 2020) 期刊论文
NATURE, 2020, 583 (7814) : 154-154
作者:  Zhang, Hao;  Liu, Chun-Xiao;  Gazibegovic, Sasa;  Xu, Di;  Logan, John A.;  Wang, Guanzhong;  van Loo, Nick;  Bommer, Jouri D. S.;  de Moor, Michiel W. A.;  Car, Diana;  Op Het Veld, Roy L. M.;  van Veldhoven, Petrus J.;  Koelling, Sebastian;  Verheijen, Marcel A.;  Pendharkar, Mihir;  Pennachio, Daniel J.;  Shojaei, Borzoyeh;  Lee, Joon Sue;  Palmstrom, Chris J.;  Bakkers, Erik P. A. M.;  Sarma, S. Das;  Kouwenhoven, Leo P.
收藏  |  浏览/下载:17/0  |  提交时间:2020/07/03
The fate of carbon in a mature forest under carbon dioxide enrichment 期刊论文
NATURE, 2020, 580 (7802) : 227-+
作者:  Sun, P. Z.;  Yang, Q.;  Kuang, W. J.;  Stebunov, Y. V.;  Xiong, W. Q.;  Yu, J.;  Nair, R. R.;  Katsnelson, M. I.;  Yuan, S. J.;  Grigorieva, I. V.;  Lozada-Hidalgo, M.;  Wang, F. C.;  Geim, A. K.
收藏  |  浏览/下载:70/0  |  提交时间:2020/05/13

Carbon dioxide enrichment of a mature forest resulted in the emission of the excess carbon back into the atmosphere via enhanced ecosystem respiration, suggesting that mature forests may be limited in their capacity to mitigate climate change.


Atmospheric carbon dioxide enrichment (eCO(2)) can enhance plant carbon uptake and growth(1-5), thereby providing an important negative feedback to climate change by slowing the rate of increase of the atmospheric CO2 concentration(6). Although evidence gathered from young aggrading forests has generally indicated a strong CO2 fertilization effect on biomass growth(3-5), it is unclear whether mature forests respond to eCO(2) in a similar way. In mature trees and forest stands(7-10), photosynthetic uptake has been found to increase under eCO(2) without any apparent accompanying growth response, leaving the fate of additional carbon fixed under eCO(2) unclear(4,5,7-11). Here using data from the first ecosystem-scale Free-Air CO2 Enrichment (FACE) experiment in a mature forest, we constructed a comprehensive ecosystem carbon budget to track the fate of carbon as the forest responded to four years of eCO(2) exposure. We show that, although the eCO(2) treatment of +150 parts per million (+38 per cent) above ambient levels induced a 12 per cent (+247 grams of carbon per square metre per year) increase in carbon uptake through gross primary production, this additional carbon uptake did not lead to increased carbon sequestration at the ecosystem level. Instead, the majority of the extra carbon was emitted back into the atmosphere via several respiratory fluxes, with increased soil respiration alone accounting for half of the total uptake surplus. Our results call into question the predominant thinking that the capacity of forests to act as carbon sinks will be generally enhanced under eCO(2), and challenge the efficacy of climate mitigation strategies that rely on ubiquitous CO2 fertilization as a driver of increased carbon sinks in global forests.


  
The projected timing of abrupt ecological disruption from climate change 期刊论文
NATURE, 2020, 580 (7804) : 496-+
作者:  Gorgulla, Christoph;  Boeszoermenyi, Andras;  Wang, Zi-Fu;  Fischer, Patrick D.;  Coote, Paul W.;  Padmanabha Das, Krishna M.;  Malets, Yehor S.;  Radchenko, Dmytro S.;  Moroz, Yurii S.;  Scott, David A.;  Fackeldey, Konstantin;  Hoffmann, Moritz;  Iavniuk, Iryna;  Wagner, Gerhard;  Arthanari, Haribabu
收藏  |  浏览/下载:56/0  |  提交时间:2020/05/13

As anthropogenic climate change continues the risks to biodiversity will increase over time, with future projections indicating that a potentially catastrophic loss of global biodiversity is on the horizon(1-3). However, our understanding of when and how abruptly this climate-driven disruption of biodiversity will occur is limited because biodiversity forecasts typically focus on individual snapshots of the future. Here we use annual projections (from 1850 to 2100) of temperature and precipitation across the ranges of more than 30,000 marine and terrestrial species to estimate the timing of their exposure to potentially dangerous climate conditions. We project that future disruption of ecological assemblages as a result of climate change will be abrupt, because within any given ecological assemblage the exposure of most species to climate conditions beyond their realized niche limits occurs almost simultaneously. Under a high-emissions scenario (representative concentration pathway (RCP) 8.5), such abrupt exposure events begin before 2030 in tropical oceans and spread to tropical forests and higher latitudes by 2050. If global warming is kept below 2 degrees C, less than 2% of assemblages globally are projected to undergo abrupt exposure events of more than 20% of their constituent species  however, the risk accelerates with the magnitude of warming, threatening 15% of assemblages at 4 degrees C, with similar levels of risk in protected and unprotected areas. These results highlight the impending risk of sudden and severe biodiversity losses from climate change and provide a framework for predicting both when and where these events may occur.


Using annual projections of temperature and precipitation to estimate when species will be exposed to potentially harmful climate conditions reveals that disruption of ecological assemblages as a result of climate change will be abrupt and could start as early as the current decade.