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Ecology: A matter of time for tropical diversity

Nature's Advance Online Publication - Wed, 2017-09-20 07:00

Nature advance online publication 20 September 2017. doi:10.1038/nature24142

Author: Gary G. Mittelbach

There is a species-diversity gradient on Earth, with the greatest diversity found near the Equator. Analysis of forest data now reveals a mechanism aiding species coexistence in the tropics that might underlie this phenomenon.

Categories: Topical E-Journals

Cancer: Drain the swamp to beat glioma

Nature's Advance Online Publication - Wed, 2017-09-20 07:00

Nature advance online publication 20 September 2017. doi:10.1038/nature24141

Authors: Michael D. Taylor & Vijay Ramaswamy

Efforts to treat brain tumours by targeting cancer cells have had only modest clinical success. It emerges that targeting a protein secreted from neurons adjacent to the tumour might be a useful alternative approach.

Categories: Topical E-Journals

Genome editing reveals a role for OCT4 in human embryogenesis

Nature's Advance Online Publication - Wed, 2017-09-20 07:00

Nature advance online publication 20 September 2017. doi:10.1038/nature24033

Authors: Norah M. E. Fogarty, Afshan McCarthy, Kirsten E. Snijders, Benjamin E. Powell, Nada Kubikova, Paul Blakeley, Rebecca Lea, Kay Elder, Sissy E. Wamaitha, Daesik Kim, Valdone Maciulyte, Jens Kleinjung, Jin-Soo Kim, Dagan Wells, Ludovic Vallier, Alessandro Bertero, James M. A. Turner & Kathy K. Niakan

Categories: Topical E-Journals

Strains, functions and dynamics in the expanded Human Microbiome Project

Nature's Advance Online Publication - Wed, 2017-09-20 07:00

Nature advance online publication 20 September 2017. doi:10.1038/nature23889

Authors: Jason Lloyd-Price, Anup Mahurkar, Gholamali Rahnavard, Jonathan Crabtree, Joshua Orvis, A. Brantley Hall, Arthur Brady, Heather H. Creasy, Carrie McCracken, Michelle G. Giglio, Daniel McDonald, Eric A. Franzosa, Rob Knight, Owen White & Curtis Huttenhower

Categories: Topical E-Journals

Axonal synapse sorting in medial entorhinal cortex

Nature's Advance Online Publication - Wed, 2017-09-20 07:00

Nature advance online publication 20 September 2017. doi:10.1038/nature24005

Authors: Helene Schmidt, Anjali Gour, Jakob Straehle, Kevin M. Boergens, Michael Brecht & Moritz Helmstaedter

Categories: Topical E-Journals

Regulation of DNA repair pathway choice in S and G2 phases by the NHEJ inhibitor CYREN

Nature's Advance Online Publication - Wed, 2017-09-20 07:00

Nature advance online publication 20 September 2017. doi:10.1038/nature24023

Authors: Nausica Arnoult, Adriana Correia, Jiao Ma, Anna Merlo, Sara Garcia-Gomez, Marija Maric, Marco Tognetti, Christopher W. Benner, Simon J. Boulton, Alan Saghatelian & Jan Karlseder

Classical non-homologous end joining (cNHEJ) and homologous recombination compete for the repair of double-stranded DNA breaks during the cell cycle. Homologous recombination is inhibited during the G1 phase of the cell cycle, but both pathways are active in the S and G2 phases. However, it is unclear why cNHEJ does not always outcompete homologous recombination during the S and G2 phases. Here we show that CYREN (cell cycle regulator of NHEJ) is a cell-cycle-specific inhibitor of cNHEJ. Suppression of CYREN allows cNHEJ to occur at telomeres and intrachromosomal breaks during the S and G2 phases, and cells lacking CYREN accumulate chromosomal aberrations upon damage induction, specifically outside the G1 phase. CYREN acts by binding to the Ku70/80 heterodimer and preferentially inhibits cNHEJ at breaks with overhangs by protecting them. We therefore propose that CYREN is a direct cell-cycle-dependent inhibitor of cNHEJ that promotes error-free repair by homologous recombination during cell cycle phases when sister chromatids are present.

Categories: Topical E-Journals

Parental influence on human germline de novo mutations in 1,548 trios from Iceland

Nature's Advance Online Publication - Wed, 2017-09-20 07:00

Nature advance online publication 20 September 2017. doi:10.1038/nature24018

Authors: Hákon Jónsson, Patrick Sulem, Birte Kehr, Snaedis Kristmundsdottir, Florian Zink, Eirikur Hjartarson, Marteinn T. Hardarson, Kristjan E. Hjorleifsson, Hannes P. Eggertsson, Sigurjon Axel Gudjonsson, Lucas D. Ward, Gudny A. Arnadottir, Einar A. Helgason, Hannes Helgason, Arnaldur Gylfason, Adalbjorg Jonasdottir, Aslaug Jonasdottir, Thorunn Rafnar, Mike Frigge, Simon N. Stacey, Olafur Th. Magnusson, Unnur Thorsteinsdottir, Gisli Masson, Augustine Kong, Bjarni V. Halldorsson, Agnar Helgason, Daniel F. Gudbjartsson & Kari Stefansson

The characterization of mutational processes that generate sequence diversity in the human genome is of paramount importance both to medical genetics and to evolutionary studies. To understand how the age and sex of transmitting parents affect de novo mutations, here we sequence 1,548 Icelanders, their parents, and, for a subset of 225, at least one child, to 35× genome-wide coverage. We find 108,778 de novo mutations, both single nucleotide polymorphisms and indels, and determine the parent of origin of 42,961. The number of de novo mutations from mothers increases by 0.37 per year of age (95% CI 0.32–0.43), a quarter of the 1.51 per year from fathers (95% CI 1.45–1.57). The number of clustered mutations increases faster with the mother’s age than with the father’s, and the genomic span of maternal de novo mutation clusters is greater than that of paternal ones. The types of de novo mutation from mothers change substantially with age, with a 0.26% (95% CI 0.19–0.33%) decrease in cytosine–phosphate–guanine to thymine–phosphate–guanine (CpG>TpG) de novo mutations and a 0.33% (95% CI 0.28–0.38%) increase in C>G de novo mutations per year, respectively. Remarkably, these age-related changes are not distributed uniformly across the genome. A striking example is a 20 megabase region on chromosome 8p, with a maternal C>G mutation rate that is up to 50-fold greater than the rest of the genome. The age-related accumulation of maternal non-crossover gene conversions also mostly occurs within these regions. Increased sequence diversity and linkage disequilibrium of C>G variants within regions affected by excess maternal mutations indicate that the underlying mutational process has persisted in humans for thousands of years. Moreover, the regional excess of C>G variation in humans is largely shared by chimpanzees, less by gorillas, and is almost absent from orangutans. This demonstrates that sequence diversity in humans results from evolving interactions between age, sex, mutation type, and genomic location.

Categories: Topical E-Journals

Layer-by-layer assembly of two-dimensional materials into wafer-scale heterostructures

Nature's Advance Online Publication - Wed, 2017-09-20 07:00

Nature advance online publication 20 September 2017. doi:10.1038/nature23905

Authors: Kibum Kang, Kan-Heng Lee, Yimo Han, Hui Gao, Saien Xie, David A. Muller & Jiwoong Park

High-performance semiconductor films with vertical compositions that are designed to atomic-scale precision provide the foundation for modern integrated circuitry and novel materials discovery. One approach to realizing such films is sequential layer-by-layer assembly, whereby atomically thin two-dimensional building blocks are vertically stacked, and held together by van der Waals interactions. With this approach, graphene and transition-metal dichalcogenides—which represent one- and three-atom-thick two-dimensional building blocks, respectively—have been used to realize previously inaccessible heterostructures with interesting physical properties. However, no large-scale assembly method exists at present that maintains the intrinsic properties of these two-dimensional building blocks while producing pristine interlayer interfaces, thus limiting the layer-by-layer assembly method to small-scale proof-of-concept demonstrations. Here we report the generation of wafer-scale semiconductor films with a very high level of spatial uniformity and pristine interfaces. The vertical composition and properties of these films are designed at the atomic scale using layer-by-layer assembly of two-dimensional building blocks under vacuum. We fabricate several large-scale, high-quality heterostructure films and devices, including superlattice films with vertical compositions designed layer-by-layer, batch-fabricated tunnel device arrays with resistances that can be tuned over four orders of magnitude, band-engineered heterostructure tunnel diodes, and millimetre-scale ultrathin membranes and windows. The stacked films are detachable, suspendable and compatible with water or plastic surfaces, which will enable their integration with advanced optical and mechanical systems.

Categories: Topical E-Journals

ApoE4 markedly exacerbates tau-mediated neurodegeneration in a mouse model of tauopathy

Nature's Advance Online Publication - Wed, 2017-09-20 07:00

Nature advance online publication 20 September 2017. doi:10.1038/nature24016

Authors: Yang Shi, Kaoru Yamada, Shane Antony Liddelow, Scott T. Smith, Lingzhi Zhao, Wenjie Luo, Richard M. Tsai, Salvatore Spina, Lea T. Grinberg, Julio C. Rojas, Gilbert Gallardo, Kairuo Wang, Joseph Roh, Grace Robinson, Mary Beth Finn, Hong Jiang, Patrick M. Sullivan, Caroline Baufeld, Michael W. Wood, Courtney Sutphen, Lena McCue, Chengjie Xiong, Jorge L. Del-Aguila, John C. Morris, Carlos Cruchaga, Anne M. Fagan, Bruce L. Miller, Adam L. Boxer, William W. Seeley, Oleg Butovsky, Ben A. Barres, Steven M. Paul & David M. Holtzman

APOE4 is the strongest genetic risk factor for late-onset Alzheimer disease. ApoE4 increases brain amyloid-? pathology relative to other ApoE isoforms. However, whether APOE independently influences tau pathology, the other major proteinopathy of Alzheimer disease and other tauopathies, or tau-mediated neurodegeneration, is not clear. By generating P301S tau transgenic mice on either a human ApoE knock-in (KI) or ApoE knockout (KO) background, here we show that P301S/E4 mice have significantly higher tau levels in the brain and a greater extent of somatodendritic tau redistribution by three months of age compared with P301S/E2, P301S/E3, and P301S/EKO mice. By nine months of age, P301S mice with different ApoE genotypes display distinct phosphorylated tau protein (p-tau) staining patterns. P301S/E4 mice develop markedly more brain atrophy and neuroinflammation than P301S/E2 and P301S/E3 mice, whereas P301S/EKO mice are largely protected from these changes. In vitro, E4-expressing microglia exhibit higher innate immune reactivity after lipopolysaccharide treatment. Co-culturing P301S tau-expressing neurons with E4-expressing mixed glia results in a significantly higher level of tumour-necrosis factor-? (TNF-?) secretion and markedly reduced neuronal viability compared with neuron/E2 and neuron/E3 co-cultures. Neurons co-cultured with EKO glia showed the greatest viability with the lowest level of secreted TNF-?. Treatment of P301S neurons with recombinant ApoE (E2, E3, E4) also leads to some neuronal damage and death compared with the absence of ApoE, with ApoE4 exacerbating the effect. In individuals with a sporadic primary tauopathy, the presence of an ?4 allele is associated with more severe regional neurodegeneration. In individuals who are positive for amyloid-? pathology with symptomatic Alzheimer disease who usually have tau pathology, ?4-carriers demonstrate greater rates of disease progression. Our results demonstrate that ApoE affects tau pathogenesis, neuroinflammation, and tau-mediated neurodegeneration independently of amyloid-? pathology. ApoE4 exerts a ‘toxic’ gain of function whereas the absence of ApoE is protective.

Categories: Topical E-Journals

Epigenetic restriction of extraembryonic lineages mirrors the somatic transition to cancer

Nature's Advance Online Publication - Wed, 2017-09-20 07:00

Nature advance online publication 20 September 2017. doi:10.1038/nature23891

Authors: Zachary D. Smith, Jiantao Shi, Hongcang Gu, Julie Donaghey, Kendell Clement, Davide Cacchiarelli, Andreas Gnirke, Franziska Michor & Alexander Meissner

In mammals, the canonical somatic DNA methylation landscape is established upon specification of the embryo proper and subsequently disrupted within many cancer types. However, the underlying mechanisms that direct this genome-scale transformation remain elusive, with no clear model for its systematic acquisition or potential developmental utility. Here, we analysed global remethylation from the mouse preimplantation embryo into the early epiblast and extraembryonic ectoderm. We show that these two states acquire highly divergent genomic distributions with substantial disruption of bimodal, CpG density-dependent methylation in the placental progenitor. The extraembryonic epigenome includes specific de novo methylation at hundreds of embryonically protected CpG island promoters, particularly those that are associated with key developmental regulators and are orthologously methylated across most human cancer types. Our data suggest that the evolutionary innovation of extraembryonic tissues may have required co-option of DNA methylation-based suppression as an alternative to regulation by Polycomb-group proteins, which coordinate embryonic germ-layer formation in response to extraembryonic cues. Moreover, we establish that this decision is made deterministically, downstream of promiscuously used—and frequently oncogenic—signalling pathways, via a novel combination of epigenetic cofactors. Methylation of developmental gene promoters during tumorigenesis may therefore reflect the misappropriation of an innate trajectory and the spontaneous reacquisition of a latent, developmentally encoded epigenetic landscape.

Categories: Topical E-Journals

Comparative glycoproteomics of stem cells identifies new players in ricin toxicity

Nature's Advance Online Publication - Wed, 2017-09-20 07:00

Nature advance online publication 20 September 2017. doi:10.1038/nature24015

Authors: Johannes Stadlmann, Jasmin Taubenschmid, Daniel Wenzel, Anna Gattinger, Gerhard Dürnberger, Frederico Dusberger, Ulrich Elling, Lukas Mach, Karl Mechtler & Josef M. Penninger

Glycosylation, the covalent attachment of carbohydrate structures onto proteins, is the most abundant post-translational modification. Over 50% of human proteins are glycosylated, which alters their activities in diverse fundamental biological processes. Despite the importance of glycosylation in biology, the identification and functional validation of complex glycoproteins has remained largely unexplored. Here we develop a novel quantitative approach to identify intact glycopeptides from comparative proteomic data sets, allowing us not only to infer complex glycan structures but also to directly map them to sites within the associated proteins at the proteome scale. We apply this method to human and mouse embryonic stem cells to illuminate the stem cell glycoproteome. This analysis nearly doubles the number of experimentally confirmed glycoproteins, identifies previously unknown glycosylation sites and multiple glycosylated stemness factors, and uncovers evolutionarily conserved as well as species-specific glycoproteins in embryonic stem cells. The specificity of our method is confirmed using sister stem cells carrying repairable mutations in enzymes required for fucosylation, Fut9 and Slc35c1. Ablation of fucosylation confers resistance to the bioweapon ricin, and we discover proteins that carry a fucosylation-dependent sugar code for ricin toxicity. Mutations disrupting a subset of these proteins render cells ricin resistant, revealing new players that orchestrate ricin toxicity. Our comparative glycoproteomics platform, SugarQb, enables genome-wide insights into protein glycosylation and glycan modifications in complex biological systems.

Categories: Topical E-Journals

Temporal coexistence mechanisms contribute to the latitudinal gradient in forest diversity

Nature's Advance Online Publication - Wed, 2017-09-20 07:00

Nature advance online publication 20 September 2017. doi:10.1038/nature24038

Authors: Jacob Usinowicz, Chia-Hao Chang-Yang, Yu-Yun Chen, James S. Clark, Christine Fletcher, Nancy C. Garwood, Zhanqing Hao, Jill Johnstone, Yiching Lin, Margaret R. Metz, Takashi Masaki, Tohru Nakashizuka, I-Fang Sun, Renato Valencia, Yunyun Wang, Jess K. Zimmerman, Anthony R. Ives & S. Joseph Wright

The tropical forests of Borneo and Amazonia may each contain more tree species diversity in half a square kilometre than do all the temperate forests of Europe, North America, and Asia combined. Biologists have long been fascinated by this disparity, using it to investigate potential drivers of biodiversity. Latitudinal variation in many of these drivers is expected to create geographic differences in ecological and evolutionary processes, and evidence increasingly shows that tropical ecosystems have higher rates of diversification, clade origination, and clade dispersal. However, there is currently no evidence to link gradients in ecological processes within communities at a local scale directly to the geographic gradient in biodiversity. Here, we show geographic variation in the storage effect, an ecological mechanism that reduces the potential for competitive exclusion more strongly in the tropics than it does in temperate and boreal zones, decreasing the ratio of interspecific-to-intraspecific competition by 0.25% for each degree of latitude that an ecosystem is located closer to the Equator. Additionally, we find evidence that latitudinal variation in climate underpins these differences; longer growing seasons in the tropics reduce constraints on the seasonal timing of reproduction, permitting lower recruitment synchrony between species and thereby enhancing niche partitioning through the storage effect. Our results demonstrate that the strength of the storage effect, and therefore its impact on diversity within communities, varies latitudinally in association with climate. This finding highlights the importance of biotic interactions in shaping geographic diversity patterns, and emphasizes the need to understand the mechanisms underpinning ecological processes in greater detail than has previously been appreciated.

Categories: Topical E-Journals

Targeting neuronal activity-regulated neuroligin-3 dependency in high-grade glioma

Nature's Advance Online Publication - Wed, 2017-09-20 07:00

Nature advance online publication 20 September 2017. doi:10.1038/nature24014

Authors: Humsa S. Venkatesh, Lydia T. Tam, Pamelyn J. Woo, James Lennon, Surya Nagaraja, Shawn M. Gillespie, Jing Ni, Damien Y. Duveau, Patrick J. Morris, Jean J. Zhao, Craig J. Thomas & Michelle Monje

High-grade gliomas (HGG) are a devastating group of cancers, and represent the leading cause of brain tumour-related death in both children and adults. Therapies aimed at mechanisms intrinsic to glioma cells have translated to only limited success; effective therapeutic strategies will need also to target elements of the tumour microenvironment that promote glioma progression. Neuronal activity promotes the growth of a range of molecularly and clinically distinct HGG types, including adult and paediatric glioblastoma (GBM), anaplastic oligodendroglioma, and diffuse intrinsic pontine glioma (DIPG). An important mechanism that mediates this neural regulation of brain cancer is activity-dependent cleavage and secretion of the synaptic adhesion molecule neuroligin-3 (NLGN3), which promotes glioma proliferation through the PI3K–mTOR pathway. However, the necessity of NLGN3 for glioma growth, the proteolytic mechanism of NLGN3 secretion, and the further molecular consequences of NLGN3 secretion in glioma cells remain unknown. Here we show that HGG growth depends on microenvironmental NLGN3, identify signalling cascades downstream of NLGN3 binding in glioma, and determine a therapeutically targetable mechanism of secretion. Patient-derived orthotopic xenografts of paediatric GBM, DIPG and adult GBM fail to grow in Nlgn3 knockout mice. NLGN3 stimulates several oncogenic pathways, such as early focal adhesion kinase activation upstream of PI3K–mTOR, and induces transcriptional changes that include upregulation of several synapse-related genes in glioma cells. NLGN3 is cleaved from both neurons and oligodendrocyte precursor cells via the ADAM10 sheddase. ADAM10 inhibitors prevent the release of NLGN3 into the tumour microenvironment and robustly block HGG xenograft growth. This work defines a promising strategy for targeting NLGN3 secretion, which could prove transformative for HGG therapy.

Categories: Topical E-Journals

Corrigendum: Stability and function of regulatory T cells expressing the transcription factor T-bet

Nature's Advance Online Publication - Wed, 2017-09-20 07:00

Nature advance online publication 20 September 2017. doi:10.1038/nature24013

Author: Andrew G. Levine, Alejandra Mendoza, Saskia Hemmers, Bruno Moltedo, Rachel E. Niec, Michail Schizas, Beatrice E. Hoyos, Ekaterina V. Putintseva, Ashutosh Chaudhry, Stanislav Dikiy, Sho Fujisawa, Dmitriy M. Chudakov, Piper M. Treuting & Alexander Y. Rudensky

Categories: Topical E-Journals

Corrigendum: High-temperature crystallization of nanocrystals into three-dimensional superlattices

Nature's Advance Online Publication - Wed, 2017-09-20 07:00

Nature advance online publication 20 September 2017. doi:10.1038/nature24025

Author: Liheng Wu, Joshua J. Willis, Ian Salmon McKay, Benjamin T. Diroll, Jian Qin, Matteo Cargnello & Christopher J. Tassone

Categories: Topical E-Journals

Corrigendum: Nuclear PKM2 regulates ?-catenin transactivation upon EGFR activation

Nature's Advance Online Publication - Wed, 2017-09-20 07:00

Nature advance online publication 20 September 2017. doi:10.1038/nature24008

Author: Weiwei Yang, Yan Xia, Haitao Ji, Yanhua Zheng, Ji Liang, Wenhua Huang, Xiang Gao, Kenneth Aldape & Zhimin Lu

Categories: Topical E-Journals

Statues: sculpting a tarnished legacy

Nature's Advance Online Publication - Mon, 2017-09-18 07:00

Nature advance online publication 18 September 2017. doi:10.1038/549334a

Author: Melinda Baldwin

Categories: Topical E-Journals

Statues: an editorial response

Nature's Advance Online Publication - Mon, 2017-09-18 07:00

Nature advance online publication 18 September 2017. doi:10.1038/549334c

Author: Philip Campbell

Categories: Topical E-Journals

Statues: researchers to mind their history

Nature's Advance Online Publication - Mon, 2017-09-18 07:00

Nature advance online publication 18 September 2017. doi:10.1038/549334b

Authors: Evelynn M. Hammonds & Susan M. Reverby

Categories: Topical E-Journals

Patchy particles made by colloidal fusion

Nature's Advance Online Publication - Mon, 2017-09-18 07:00

Nature advance online publication 18 September 2017. doi:10.1038/nature23901

Authors: Zhe Gong, Theodore Hueckel, Gi-Ra Yi & Stefano Sacanna

Patches on the surfaces of colloidal particles provide directional information that enables the self-assembly of the particles into higher-order structures. Although computational tools can make quantitative predictions and can generate design rules that link the patch motif of a particle to its internal microstructure and to the emergent properties of the self-assembled materials, the experimental realization of model systems of particles with surface patches (or ‘patchy’ particles) remains a challenge. Synthetic patchy colloidal particles are often poor geometric approximations of the digital building blocks used in simulations and can only rarely be manufactured in sufficiently high yields to be routinely used as experimental model systems. Here we introduce a method, which we refer to as colloidal fusion, for fabricating functional patchy particles in a tunable and scalable manner. Using coordination dynamics and wetting forces, we engineer hybrid liquid–solid clusters that evolve into particles with a range of patchy surface morphologies on addition of a plasticizer. We are able to predict and control the evolutionary pathway by considering surface-energy minimization, leading to two main branches of product: first, spherical particles with liquid surface patches, capable of forming curable bonds with neighbouring particles to assemble robust supracolloidal structures; and second, particles with a faceted liquid compartment, which can be cured and purified to yield colloidal polyhedra. These findings outline a scalable strategy for the synthesis of patchy particles, first by designing their surface patterns by computer simulation, and then by recreating them in the laboratory with high fidelity.

Categories: Topical E-Journals
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