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Nature is the international weekly journal of science: a magazine style journal that publishes full-length research papers in all disciplines of science, as well as News and Views, reviews, news, features, commentaries, web focuses and more, covering all branches of science and how science impacts upon all aspects of society and life.
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Structures of the calcium-activated, non-selective cation channel TRPM4

Wed, 12/06/2017 - 01:00

Structures of the calcium-activated, non-selective cation channel TRPM4

Nature 552, 7684 (2017). doi:10.1038/nature24997

Authors: Jiangtao Guo, Ji She, Weizhong Zeng, Qingfeng Chen, Xiao-chen Bai & Youxing Jiang

TRPM4 is a calcium-activated, phosphatidylinositol-4,5-bisphosphate (PtdIns(4,5)P2) -modulated, non-selective cation channel that belongs to the family of melastatin-related transient receptor potential (TRPM) channels. Here we present the electron cryo-microscopy structures of the mouse TRPM4 channel with and without ATP. TRPM4 consists of multiple transmembrane

Categories: Literature

Force loading explains spatial sensing of ligands by cells

Wed, 12/06/2017 - 01:00

Force loading explains spatial sensing of ligands by cells

Nature 552, 7684 (2017). doi:10.1038/nature24662

Authors: Roger Oria, Tina Wiegand, Jorge Escribano, Alberto Elosegui-Artola, Juan Jose Uriarte, Cristian Moreno-Pulido, Ilia Platzman, Pietro Delcanale, Lorenzo Albertazzi, Daniel Navajas, Xavier Trepat, José Manuel García-Aznar, Elisabetta Ada Cavalcanti-Adam & Pere Roca-Cusachs

Cells can sense the density and distribution of extracellular matrix (ECM) molecules by means of individual integrin proteins and larger, integrin-containing adhesion complexes within the cell membrane. This spatial sensing drives cellular activity in a variety of normal and pathological contexts. Previous studies of cells on rigid glass surfaces have shown that spatial sensing of ECM ligands takes place at the nanometre scale, with integrin clustering and subsequent formation of focal adhesions impaired when single integrin–ligand bonds are separated by more than a few tens of nanometres. It has thus been suggested that a crosslinking ‘adaptor’ protein of this size might connect integrins to the actin cytoskeleton, acting as a molecular ruler that senses ligand spacing directly. Here, we develop gels whose rigidity and nanometre-scale distribution of ECM ligands can be controlled and altered. We find that increasing the spacing between ligands promotes the growth of focal adhesions on low-rigidity substrates, but leads to adhesion collapse on more-rigid substrates. Furthermore, disordering the ligand distribution drastically increases adhesion growth, but reduces the rigidity threshold for adhesion collapse. The growth and collapse of focal adhesions are mirrored by, respectively, the nuclear or cytosolic localization of the transcriptional regulator protein YAP. We explain these findings not through direct sensing of ligand spacing, but by using an expanded computational molecular-clutch model, in which individual integrin–ECM bonds—the molecular clutches—respond to force loading by recruiting extra integrins, up to a maximum value. This generates more clutches, redistributing the overall force among them, and reducing the force loading per clutch. At high rigidity and high ligand spacing, maximum recruitment is reached, preventing further force redistribution and leading to adhesion collapse. Measurements of cellular traction forces and actin flow speeds support our model. Our results provide a general framework for how cells sense spatial and physical information at the nanoscale, precisely tuning the range of conditions at which they form adhesions and activate transcriptional regulation.

Categories: Literature

Moving beyond microbiome-wide associations to causal microbe identification

Wed, 12/06/2017 - 01:00

Moving beyond microbiome-wide associations to causal microbe identification

Nature 552, 7684 (2017). doi:10.1038/nature25019

Authors: Neeraj K. Surana & Dennis L. Kasper

Microbiome-wide association studies have established that numerous diseases are associated with changes in the microbiota. These studies typically generate a long list of commensals implicated as biomarkers of disease, with no clear relevance to disease pathogenesis. If the field is to move beyond correlations and begin to address causation, an effective system is needed for refining this catalogue of differentially abundant microbes and to allow subsequent mechanistic studies. Here we demonstrate that triangulation of microbe–phenotype relationships is an effective method for reducing the noise inherent in microbiota studies and enabling identification of causal microbes. We found that gnotobiotic mice harbouring different microbial communities exhibited differential survival in a colitis model. Co-housing of these mice generated animals that had hybrid microbiotas and displayed intermediate susceptibility to colitis. Mapping of microbe–phenotype relationships in parental mouse strains and in mice with hybrid microbiotas identified the bacterial family Lachnospiraceae as a correlate for protection from disease. Using directed microbial culture techniques, we discovered Clostridium immunis, a previously unknown bacterial species from this family, that—when administered to colitis-prone mice—protected them against colitis-associated death. To demonstrate the generalizability of our approach, we used it to identify several commensal organisms that induce intestinal expression of an antimicrobial peptide. Thus, we have used microbe–phenotype triangulation to move beyond the standard correlative microbiome study and identify causal microbes for two completely distinct phenotypes. Identification of disease-modulating commensals by microbe–phenotype triangulation may be more broadly applicable to human microbiome studies.

Categories: Literature

Inhibition of soluble epoxide hydrolase prevents diabetic retinopathy

Wed, 12/06/2017 - 01:00

Inhibition of soluble epoxide hydrolase prevents diabetic retinopathy

Nature 552, 7684 (2017). doi:10.1038/nature25013

Authors: Jiong Hu, Sarah Dziumbla, Jihong Lin, Sofia-Iris Bibli, Sven Zukunft, Julian de Mos, Khader Awwad, Timo Frömel, Andreas Jungmann, Kavi Devraj, Zhixing Cheng, Liya Wang, Sascha Fauser, Charles G. Eberhart, Akrit Sodhi, Bruce D. Hammock, Stefan Liebner, Oliver J. Müller, Clemens Glaubitz, Hans-Peter Hammes, Rüdiger Popp & Ingrid Fleming

Diabetic retinopathy is an important cause of blindness in adults, and is characterized by progressive loss of vascular cells and slow dissolution of inter-vascular junctions, which result in vascular leakage and retinal oedema. Later stages of the disease are characterized by inflammatory cell infiltration, tissue destruction and neovascularization. Here we identify soluble epoxide hydrolase (sEH) as a key enzyme that initiates pericyte loss and breakdown of endothelial barrier function by generating the diol 19,20-dihydroxydocosapentaenoic acid, derived from docosahexaenoic acid. The expression of sEH and the accumulation of 19,20-dihydroxydocosapentaenoic acid were increased in diabetic mouse retinas and in the retinas and vitreous humour of patients with diabetes. Mechanistically, the diol targeted the cell membrane to alter the localization of cholesterol-binding proteins, and prevented the association of presenilin 1 with N-cadherin and VE-cadherin, thereby compromising pericyte–endothelial cell interactions and inter-endothelial cell junctions. Treating diabetic mice with a specific sEH inhibitor prevented the pericyte loss and vascular permeability that are characteristic of non-proliferative diabetic retinopathy. Conversely, overexpression of sEH in the retinal Müller glial cells of non-diabetic mice resulted in similar vessel abnormalities to those seen in diabetic mice with retinopathy. Thus, increased expression of sEH is a key determinant in the pathogenesis of diabetic retinopathy, and inhibition of sEH can prevent progression of the disease.

Categories: Literature

Runx3 programs CD8+ T cell residency in non-lymphoid tissues and tumours

Wed, 12/06/2017 - 01:00

Runx3 programs CD8+ T cell residency in non-lymphoid tissues and tumours

Nature 552, 7684 (2017). doi:10.1038/nature24993

Authors: J. Justin Milner, Clara Toma, Bingfei Yu, Kai Zhang, Kyla Omilusik, Anthony T. Phan, Dapeng Wang, Adam J. Getzler, Toan Nguyen, Shane Crotty, Wei Wang, Matthew E. Pipkin & Ananda W. Goldrath

Tissue-resident memory CD8+ T (TRM) cells are found at common sites of pathogen exposure, where they elicit rapid and robust protective immune responses. However, the molecular signals that control TRM cell differentiation and homeostasis are not fully understood. Here we show that mouse TRM precursor cells represent a unique CD8+ T cell subset that is distinct from the precursors of circulating memory cell populations at the levels of gene expression and chromatin accessibility. Using computational and pooled in vivo RNA interference screens, we identify the transcription factor Runx3 as a key regulator of TRM cell differentiation and homeostasis. Runx3 was required to establish TRM cell populations in diverse tissue environments, and supported the expression of crucial tissue-residency genes while suppressing genes associated with tissue egress and recirculation. Furthermore, we show that human and mouse tumour-infiltrating lymphocytes share a core tissue-residency gene-expression signature with TRM cells that is associated with Runx3 activity. In a mouse model of adoptive T cell therapy for melanoma, Runx3-deficient CD8+ tumour-infiltrating lymphocytes failed to accumulate in tumours, resulting in greater rates of tumour growth and mortality. Conversely, overexpression of Runx3 enhanced tumour-specific CD8+ T cell abundance, delayed tumour growth, and prolonged survival. In addition to establishing Runx3 as a central regulator of TRM cell differentiation, these results provide insight into the signals that promote T cell residency in non-lymphoid sites, which could be used to enhance vaccine efficacy or adoptive cell therapy treatments that target cancer.

Categories: Literature

piRNA-mediated regulation of transposon alternative splicing in the soma and germ line

Wed, 12/06/2017 - 01:00

piRNA-mediated regulation of transposon alternative splicing in the soma and germ line

Nature 552, 7684 (2017). doi:10.1038/nature25018

Authors: Felipe Karam Teixeira, Martyna Okuniewska, Colin D. Malone, Rémi-Xavier Coux, Donald C. Rio & Ruth Lehmann

Transposable elements can drive genome evolution, but their enhanced activity is detrimental to the host and therefore must be tightly regulated. The Piwi-interacting small RNA (piRNA) pathway is vital for the regulation of transposable elements, by inducing transcriptional silencing or post-transcriptional decay of mRNAs. Here we show that piRNAs and piRNA biogenesis components regulate precursor mRNA splicing of P-transposable element transcripts in vivo, leading to the production of the non-transposase-encoding mature mRNA isoform in Drosophila germ cells. Unexpectedly, we show that the piRNA pathway components do not act to reduce transcript levels of the P-element transposon during P–M hybrid dysgenesis, a syndrome that affects germline development in Drosophila. Instead, splicing regulation is mechanistically achieved together with piRNA-mediated changes to repressive chromatin states, and relies on the function of the Piwi–piRNA complex proteins Asterix (also known as Gtsf1) and Panoramix (Silencio), as well as Heterochromatin protein 1a (HP1a; encoded by Su(var)205). Furthermore, we show that this machinery, together with the piRNA Flamenco cluster, not only controls the accumulation of Gypsy retrotransposon transcripts but also regulates the splicing of Gypsy mRNAs in cultured ovarian somatic cells, a process required for the production of infectious particles that can lead to heritable transposition events. Our findings identify splicing regulation as a new role and essential function for the Piwi pathway in protecting the genome against transposon mobility, and provide a model system for studying the role of chromatin structure in modulating alternative splicing during development.

Categories: Literature

KAT2A coupled with the α-KGDH complex acts as a histone H3 succinyltransferase

Wed, 12/06/2017 - 01:00

KAT2A coupled with the α-KGDH complex acts as a histone H3 succinyltransferase

Nature 552, 7684 (2017). doi:10.1038/nature25003

Authors: Yugang Wang, Yusong R. Guo, Ke Liu, Zheng Yin, Rui Liu, Yan Xia, Lin Tan, Peiying Yang, Jong-Ho Lee, Xin-jian Li, David Hawke, Yanhua Zheng, Xu Qian, Jianxin Lyu, Jie He, Dongming Xing, Yizhi Jane Tao & Zhimin Lu

Histone modifications, such as the frequently occurring lysine succinylation, are central to the regulation of chromatin-based processes. However, the mechanism and functional consequences of histone succinylation are unknown. Here we show that the α-ketoglutarate dehydrogenase (α-KGDH) complex is localized in the nucleus in human cell lines and binds to lysine acetyltransferase 2A (KAT2A, also known as GCN5) in the promoter regions of genes. We show that succinyl-coenzyme A (succinyl-CoA) binds to KAT2A. The crystal structure of the catalytic domain of KAT2A in complex with succinyl-CoA at 2.3 Å resolution shows that succinyl-CoA binds to a deep cleft of KAT2A with the succinyl moiety pointing towards the end of a flexible loop 3, which adopts different structural conformations in succinyl-CoA-bound and acetyl-CoA-bound forms. Site-directed mutagenesis indicates that tyrosine 645 in this loop has an important role in the selective binding of succinyl-CoA over acetyl-CoA. KAT2A acts as a succinyltransferase and succinylates histone H3 on lysine 79, with a maximum frequency around the transcription start sites of genes. Preventing the α-KGDH complex from entering the nucleus, or expression of KAT2A(Tyr645Ala), reduces gene expression and inhibits tumour cell proliferation and tumour growth. These findings reveal an important mechanism of histone modification and demonstrate that local generation of succinyl-CoA by the nuclear α-KGDH complex coupled with the succinyltransferase activity of KAT2A is instrumental in histone succinylation, tumour cell proliferation, and tumour development.

Categories: Literature

Greater future global warming inferred from Earth’s recent energy budget

Wed, 12/06/2017 - 01:00

Greater future global warming inferred from Earth’s recent energy budget

Nature 552, 7683 (2017). doi:10.1038/nature24672

Authors: Patrick T. Brown & Ken Caldeira

Climate models provide the principal means of projecting global warming over the remainder of the twenty-first century but modelled estimates of warming vary by a factor of approximately two even under the same radiative forcing scenarios. Across-model relationships between currently observable attributes of the climate

Categories: Literature

Fractal assembly of micrometre-scale DNA origami arrays with arbitrary patterns

Wed, 12/06/2017 - 01:00

Fractal assembly of micrometre-scale DNA origami arrays with arbitrary patterns

Nature 552, 7683 (2017). doi:10.1038/nature24655

Authors: Grigory Tikhomirov, Philip Petersen & Lulu Qian

Self-assembled DNA nanostructures enable nanometre-precise patterning that can be used to create programmable molecular machines and arrays of functional materials. DNA origami is particularly versatile in this context because each DNA strand in the origami nanostructure occupies a unique position and can serve as a uniquely addressable pixel. However, the scale of such structures has been limited to about 0.05 square micrometres, hindering applications that demand a larger layout and integration with more conventional patterning methods. Hierarchical multistage assembly of simple sets of tiles can in principle overcome this limitation, but so far has not been sufficiently robust to enable successful implementation of larger structures using DNA origami tiles. Here we show that by using simple local assembly rules that are modified and applied recursively throughout a hierarchical, multistage assembly process, a small and constant set of unique DNA strands can be used to create DNA origami arrays of increasing size and with arbitrary patterns. We illustrate this method, which we term ‘fractal assembly’, by producing DNA origami arrays with sizes of up to 0.5 square micrometres and with up to 8,704 pixels, allowing us to render images such as the Mona Lisa and a rooster. We find that self-assembly of the tiles into arrays is unaffected by changes in surface patterns on the tiles, and that the yield of the fractal assembly process corresponds to about 0.95m − 1 for arrays containing m tiles. When used in conjunction with a software tool that we developed that converts an arbitrary pattern into DNA sequences and experimental protocols, our assembly method is readily accessible and will facilitate the construction of sophisticated materials and devices with sizes similar to that of a bacterium using DNA nanostructures.

Categories: Literature

Programmable self-assembly of three-dimensional nanostructures from 10,000 unique components

Wed, 12/06/2017 - 01:00

Programmable self-assembly of three-dimensional nanostructures from 10,000 unique components

Nature 552, 7683 (2017). doi:10.1038/nature24648

Authors: Luvena L. Ong, Nikita Hanikel, Omar K. Yaghi, Casey Grun, Maximilian T. Strauss, Patrick Bron, Josephine Lai-Kee-Him, Florian Schueder, Bei Wang, Pengfei Wang, Jocelyn Y. Kishi, Cameron Myhrvold, Allen Zhu, Ralf Jungmann, Gaetan Bellot, Yonggang Ke & Peng Yin

Nucleic acids (DNA and RNA) are widely used to construct nanometre-scale structures with ever increasing complexity, with possible application in fields such as structural biology, biophysics, synthetic biology and photonics. The nanostructures are formed through one-pot self-assembly, with early kilodalton-scale examples containing typically tens of unique DNA strands. The introduction of DNA origami, which uses many staple strands to fold one long scaffold strand into a desired structure, has provided access to megadalton-scale nanostructures that contain hundreds of unique DNA strands. Even larger DNA origami structures are possible, but manufacturing and manipulating an increasingly long scaffold strand remains a challenge. An alternative and more readily scalable approach involves the assembly of DNA bricks, which each consist of four short binding domains arranged so that the bricks can interlock. This approach does not require a scaffold; instead, the short DNA brick strands self-assemble according to specific inter-brick interactions. First-generation bricks used to create three-dimensional structures are 32 nucleotides long, consisting of four eight-nucleotide binding domains. Protocols have been designed to direct the assembly of hundreds of distinct bricks into well formed structures, but attempts to create larger structures have encountered practical challenges and had limited success. Here we show that DNA bricks with longer, 13-nucleotide binding domains make it possible to self-assemble 0.1–1-gigadalton, three-dimensional nanostructures from tens of thousands of unique components, including a 0.5-gigadalton cuboid containing about 30,000 unique bricks and a 1-gigadalton rotationally symmetric tetramer. We also assembled a cuboid that contains around 10,000 bricks and about 20,000 uniquely addressable, 13-base-pair ‘voxels’ that serves as a molecular canvas for three-dimensional sculpting. Complex, user-prescribed, three-dimensional cavities can be produced within this molecular canvas, enabling the creation of shapes such as letters, a helicoid and a teddy bear. We anticipate that with further optimization of structure design, strand synthesis and assembly procedure even larger structures could be accessible, which could be useful for applications such as positioning functional components.

Categories: Literature

Gigadalton-scale shape-programmable DNA assemblies

Wed, 12/06/2017 - 01:00

Gigadalton-scale shape-programmable DNA assemblies

Nature 552, 7683 (2017). doi:10.1038/nature24651

Authors: Klaus F. Wagenbauer, Christian Sigl & Hendrik Dietz

Natural biomolecular assemblies such as molecular motors, enzymes, viruses and subcellular structures often form by self-limiting hierarchical oligomerization of multiple subunits. Large structures can also assemble efficiently from a few components by combining hierarchical assembly and symmetry, a strategy exemplified by viral capsids. De novo protein design and RNA and DNA nanotechnology aim to mimic these capabilities, but the bottom-up construction of artificial structures with the dimensions and complexity of viruses and other subcellular components remains challenging. Here we show that natural assembly principles can be combined with the methods of DNA origami to produce gigadalton-scale structures with controlled sizes. DNA sequence information is used to encode the shapes of individual DNA origami building blocks, and the geometry and details of the interactions between these building blocks then control their copy numbers, positions and orientations within higher-order assemblies. We illustrate this strategy by creating planar rings of up to 350 nanometres in diameter and with atomic masses of up to 330 megadaltons, micrometre-long, thick tubes commensurate in size to some bacilli, and three-dimensional polyhedral assemblies with sizes of up to 1.2 gigadaltons and 450 nanometres in diameter. We achieve efficient assembly, with yields of up to 90 per cent, by using building blocks with validated structure and sufficient rigidity, and an accurate design with interaction motifs that ensure that hierarchical assembly is self-limiting and able to proceed in equilibrium to allow for error correction. We expect that our method, which enables the self-assembly of structures with sizes approaching that of viruses and cellular organelles, can readily be used to create a range of other complex structures with well defined sizes, by exploiting the modularity and high degree of addressability of the DNA origami building blocks used.

Categories: Literature

Biotechnological mass production of DNA origami

Wed, 12/06/2017 - 01:00

Biotechnological mass production of DNA origami

Nature 552, 7683 (2017). doi:10.1038/nature24650

Authors: Florian Praetorius, Benjamin Kick, Karl L. Behler, Maximilian N. Honemann, Dirk Weuster-Botz & Hendrik Dietz

DNA nanotechnology, in particular DNA origami, enables the bottom-up self-assembly of micrometre-scale, three-dimensional structures with nanometre-precise features. These structures are customizable in that they can be site-specifically functionalized or constructed to exhibit machine-like or logic-gating behaviour. Their use has been limited to applications that require only small amounts of material (of the order of micrograms), owing to the limitations of current production methods. But many proposed applications, for example as therapeutic agents or in complex materials, could be realized if more material could be used. In DNA origami, a nanostructure is assembled from a very long single-stranded scaffold molecule held in place by many short single-stranded staple oligonucleotides. Only the bacteriophage-derived scaffold molecules are amenable to scalable and efficient mass production; the shorter staple strands are obtained through costly solid-phase synthesis or enzymatic processes. Here we show that single strands of DNA of virtually arbitrary length and with virtually arbitrary sequences can be produced in a scalable and cost-efficient manner by using bacteriophages to generate single-stranded precursor DNA that contains target strand sequences interleaved with self-excising ‘cassettes’, with each cassette comprising two Zn2+-dependent DNA-cleaving DNA enzymes. We produce all of the necessary single strands of DNA for several DNA origami using shaker-flask cultures, and demonstrate end-to-end production of macroscopic amounts of a DNA origami nanorod in a litre-scale stirred-tank bioreactor. Our method is compatible with existing DNA origami design frameworks and retains the modularity and addressability of DNA origami objects that are necessary for implementing custom modifications using functional groups. With all of the production and purification steps amenable to scaling, we expect that our method will expand the scope of DNA nanotechnology in many areas of science and technology.

Categories: Literature

Primordial clays on Mars formed beneath a steam or supercritical atmosphere

Wed, 12/06/2017 - 01:00

Primordial clays on Mars formed beneath a steam or supercritical atmosphere

Nature 552, 7683 (2017). doi:10.1038/nature24657

Authors: Kevin M. Cannon, Stephen W. Parman & John F. Mustard

On Mars, clay minerals are widespread in terrains that date back to the Noachian period (4.1 billion to 3.7 billion years ago). It is thought that the Martian basaltic crust reacted with liquid water during this time to form hydrated clay minerals. Here we propose, however, that a substantial proportion of these clays was formed when Mars’ primary crust reacted with a dense steam or supercritical atmosphere of water and carbon dioxide that was outgassed during magma ocean cooling. We present experimental evidence that shows rapid clay formation under conditions that would have been present at the base of such an atmosphere and also deeper in the porous crust. Furthermore, we explore the fate of a primordial clay-rich layer with the help of a parameterized crustal evolution model; we find that the primordial clay is locally disrupted by impacts and buried by impact-ejected material and by erupted volcanic material, but that it survives as a mostly coherent layer at depth, with limited surface exposures. These exposures are similar to those observed in remotely sensed orbital data from Mars. Our results can explain the present distribution of many clays on Mars, and the anomalously low density of the Martian crust in comparison with expectations.

Categories: Literature

Large emissions from floodplain trees close the Amazon methane budget

Mon, 12/04/2017 - 01:00

Large emissions from floodplain trees close the Amazon methane budget

Nature 552, 7684 (2017). doi:10.1038/nature24639

Authors: Sunitha R. Pangala, Alex Enrich-Prast, Luana S. Basso, Roberta Bittencourt Peixoto, David Bastviken, Edward R. C. Hornibrook, Luciana V. Gatti, Humberto Marotta, Luana Silva Braucks Calazans, Cassia Mônica Sakuragui, Wanderley Rodrigues Bastos, Olaf Malm, Emanuel Gloor, John Bharat Miller & Vincent Gauci

Wetlands are the largest global source of atmospheric methane (CH4), a potent greenhouse gas. However, methane emission inventories from the Amazon floodplain, the largest natural geographic source of CH4 in the tropics, consistently underestimate the atmospheric burden of CH4 determined via remote sensing and inversion modelling, pointing to a major gap in our understanding of the contribution of these ecosystems to CH4 emissions. Here we report CH4 fluxes from the stems of 2,357 individual Amazonian floodplain trees from 13 locations across the central Amazon basin. We find that escape of soil gas through wetland trees is the dominant source of regional CH4 emissions. Methane fluxes from Amazon tree stems were up to 200 times larger than emissions reported for temperate wet forests and tropical peat swamp forests, representing the largest non-ebullitive wetland fluxes observed. Emissions from trees had an average stable carbon isotope value (δ13C) of −66.2 ± 6.4 per mil, consistent with a soil biogenic origin. We estimate that floodplain trees emit 15.1 ± 1.8 to 21.2 ± 2.5 teragrams of CH4 a year, in addition to the 20.5 ± 5.3 teragrams a year emitted regionally from other sources. Furthermore, we provide a ‘top-down’ regional estimate of CH4 emissions of 42.7 ± 5.6 teragrams of CH4 a year for the Amazon basin, based on regular vertical lower-troposphere CH4 profiles covering the period 2010–2013. We find close agreement between our ‘top-down’ and combined ‘bottom-up’ estimates, indicating that large CH4 emissions from trees adapted to permanent or seasonal inundation can account for the emission source that is required to close the Amazon CH4 budget. Our findings demonstrate the importance of tree stem surfaces in mediating approximately half of all wetland CH4 emissions in the Amazon floodplain, a region that represents up to one-third of the global wetland CH4 source when trees are combined with other emission sources.

Categories: Literature

Huge haul of rare pterosaur eggs excites palaeontologists

Thu, 11/30/2017 - 01:00

Huge haul of rare pterosaur eggs excites palaeontologists

Nature 552, 7683 (2017). http://www.nature.com/doifinder/10.1038/nature.2017.23049

Author: John Pickrell

Embryos found in some fossil eggs suggest that hatchlings struggled to fly.

Categories: Literature

Research health needs a dedicated group

Wed, 11/29/2017 - 01:00

Research health needs a dedicated group

Nature 551, 7681 (2017). doi:10.1038/d41586-017-07330-5

Author:

A US Research Integrity Advisory Board is long overdue. Such a leadership body would mitigate bad practices and strengthen good research.

Categories: Literature

As climate talks end, it is time for action 

Wed, 11/29/2017 - 01:00

As climate talks end, it is time for action 

Nature 551, 7681 (2017). doi:10.1038/d41586-017-07273-x

Author:

Worrying disconnect between emissions rhetoric and real-world trends highlights urgent need for nations to honour their pledges.

Categories: Literature

Rewarding negative results keeps science on track

Wed, 11/29/2017 - 01:00

Rewarding negative results keeps science on track

Nature 551, 7681 (2017). doi:10.1038/d41586-017-07325-2

Author:

Creating a culture of replication takes prizes, grants and magnanimity — as well as publications.

Categories: Literature

We can and must govern climate engineering 

Wed, 11/29/2017 - 01:00

We can and must govern climate engineering 

Nature 551, 7681 (2017). http://www.nature.com/doifinder/10.1038/d41586-017-07296-4

Author: Stephen O. Andersen

Use the Montreal Protocol to manage controversial work intended to limit global warming, urges Stephen O. Andersen.

Categories: Literature

Exoplanet find, oil pipeline and a gene-editing first

Wed, 11/29/2017 - 01:00

Exoplanet find, oil pipeline and a gene-editing first

Nature 551, 7681 (2017). http://www.nature.com/doifinder/10.1038/d41586-017-07363-w

Author:

The week in science: 17–23 November 2017.

Categories: Literature

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