Beyond EICA : understanding post-establishment evolution requires a broader evaluation of potential selection pressures

Research on post-establishment evolution in nonnative plant populations has focused almost exclusively on testing the Evolution of Increased Competitive Ability (EICA) hypothesis, which posits that the lack of specialized herbivores in the invaded range drives evolution in nonnative plant populations. Fifteen years of conflicting EICA test results suggest that selection pressures other than specialized herbivory are important in driving post-establishment evolution in invasive species. Alternative hypotheses, such as the Evolution of Reduced Competitive Ability (ERCA) hypothesis, have been proposed but have received little attention or testing. We argue that the lack of consensus across studies that test EICA may be due in part to the lack of consistent definitions and varying experimental design parameters, and that future research in this field would benefit from new methodological considerations. We examined previous work evaluating post-establishment evolution and evaluated the range of study systems and design parameters used in testing the EICA hypothesis. Our goal was to identify where different uses of ecological terms and different study parameters have hindered consensus and to suggest a path forward to move beyond EICA in post-establishment evolution studies. We incorporated these methods into a design framework that will increase data harmony across future studies and will facilitate examinations of any potential selection pressure driving evolution in the invaded range

Joining Together to Build More: The New England Software Carpentry Library Consortium

In 2017 a group of academic library and information technology staff from institutions across New England piloted a process of joining The Carpentries, an organization developed to train researchers in essential computing skills and practices for automating and improving their handling of data, as a consortium. The New England Software Carpentry Library Consortium (NESCLiC) shared a gold-level tier membership to become a Carpentries member organization. NESCLiC members attended a Software Carpentry workshop together and then participated in instructor training as a cohort, collaborating on learning the material, practicing, and beginning to host and teach workshops as a group. This article describes both the successes and challenges of forming this new consortium, suggests good practices for those who might wish to form similar collaborations, and discusses the future of this program and other efforts to help researchers improve their computing and data handling skills

Marine Reserves Shape Seascapes on Scales Visible From Space

Marine reserves can effectively restore harvested populations, and ‘mega-reserves’ increasingly protect large tracts of ocean. However, no method exists of monitoring ecological responses at this large scale. Herbivory is a key mechanism structuring ecosystems, and this consumer–resource interaction\u27s strength on coral reefs can indicate ecosystem health. We screened 1372, and measured features of 214, reefs throughout Australia\u27s Great Barrier Reef using high-resolution satellite imagery, combined with remote underwater videography and assays on a subset, to quantify the prevalence, size and potential causes of ‘grazing halos’. Halos are known to be seascape-scale footprints of herbivory and other ecological interactions. Here we show that these halo-like footprints are more prevalent in reserves, particularly older ones (approx. 40 years old), resulting in predictable changes to reef habitat at scales visible from space. While the direct mechanisms for this pattern are relatively clear, the indirect mechanisms remain untested. By combining remote sensing and behavioural ecology, our findings demonstrate that reserves can shape large-scale habitat structure by altering herbivores\u27 functional importance, suggesting that reserves may have greater value in restoring ecosystems than previously appreciated. Additionally, our results show that we can now detect macro-patterns in reef species interactions using freely available satellite imagery. Low-cost, ecosystem-level observation tools will be critical as reserves increase in number and scope; further investigation into whether halos may help seems warranted. Significance statement: Marine reserves are a widely used tool to mitigate fishing impacts on marine ecosystems. Predicting reserves\u27 large-scale effects on habitat structure and ecosystem functioning is a major challenge, however, because these effects unfold over longer and larger scales than most ecological studies. We use a unique approach merging remote sensing and behavioural ecology to detect ecosystem change within reserves in Australia\u27s vast Great Barrier Reef. We find evidence of changes in reefs\u27 algal habitat structure occurring over large spatial (thousands of kilometres) and temporal (40+ years) scales, demonstrating that reserves can alter herbivory and habitat structure in predictable ways. This approach demonstrates that we can now detect aspects of reefs\u27 ecological responses to protection even in remote and inaccessible reefs globally

A new CP violating observable for the LHC

We study a new type of CP violating observable that arises in three body decays that are dominated by an intermediate resonance. If two interfering diagrams exist with different orderings of final state particles, the required CP-even phase arises due to the different virtualities of the resonance in each of the two diagrams. This method can be an important tool for accessing new CP phases at the LHC and future colliders.Comment: 22 pages, v2: discussion of charged particle decays and a few references added v3: typos corrected, matches published versio

Site-Specific Metal Chelation Facilitates the Unveiling of Hidden Coordination Sites in an Fe II/Fe III -Seamed Pyrogallol[4]arene Nanocapsule

Under suitable conditions, C-alkylpyrogallol­[4]­arenes (PgCs) arrange into spherical metal–organic nanocapsules (MONCs) upon coordination to appropriate metal ions. Herein we present the synthesis and structural characterization of a novel FeII/FeIII-seamed MONC, as well as studies related to its electrochemical and magnetic behaviors. Unlike other MONCs that are assembled through 24 metal ions, this nanocapsule comprises 32 Fe ions, uncovering 8 additional coordination sites situated between the constituent PgC subunits. The FeII ions are likely formed by the reducing ability of DMF used in the synthesis, representing a novel synthetic route toward polynuclear mixed-valence MONCs

Fermi Large Area Telescope Constraints on the Gamma-ray Opacity of the Universe

The Extragalactic Background Light (EBL) includes photons with wavelengths from ultraviolet to infrared, which are effective at attenuating gamma rays with energy above ~10 GeV during propagation from sources at cosmological distances. This results in a redshift- and energy-dependent attenuation of the gamma-ray flux of extragalactic sources such as blazars and Gamma-Ray Bursts (GRBs). The Large Area Telescope onboard Fermi detects a sample of gamma-ray blazars with redshift up to z~3, and GRBs with redshift up to z~4.3. Using photons above 10 GeV collected by Fermi over more than one year of observations for these sources, we investigate the effect of gamma-ray flux attenuation by the EBL. We place upper limits on the gamma-ray opacity of the Universe at various energies and redshifts, and compare this with predictions from well-known EBL models. We find that an EBL intensity in the optical-ultraviolet wavelengths as great as predicted by the "baseline" model of Stecker et al. (2006) can be ruled out with high confidence.Comment: 42 pages, 12 figures, accepted version (24 Aug.2010) for publication in ApJ; Contact authors: A. Bouvier, A. Chen, S. Raino, S. Razzaque, A. Reimer, L.C. Reye

Hundreds of variants clustered in genomic loci and biological pathways affect human height

Most common human traits and diseases have a polygenic pattern of inheritance: DNA sequence variants at many genetic loci influence the phenotype. Genome-wide association (GWA) studies have identified more than 600 variants associated with human traits, but these typically explain small fractions of phenotypic variation, raising questions about the use of further studies. Here, using 183,727 individuals, we show that hundreds of genetic variants, in at least 180 loci, influence adult height, a highly heritable and classic polygenic trait. The large number of loci reveals patterns with important implications for genetic studies of common human diseases and traits. First, the 180 loci are not random, but instead are enriched for genes that are connected in biological pathways (P = 0.016) and that underlie skeletal growth defects (P < 0.001). Second, the likely causal gene is often located near the most strongly associated variant: in 13 of 21 loci containing a known skeletal growth gene, that gene was closest to the associated variant. Third, at least 19 loci have multiple independently associated variants, suggesting that allelic heterogeneity is a frequent feature of polygenic traits, that comprehensive explorations of already-discovered loci should discover additional variants and that an appreciable fraction of associated loci may have been identified. Fourth, associated variants are enriched for likely functional effects on genes, being over-represented among variants that alter amino-acid structure of proteins and expression levels of nearby genes. Our data explain approximately 10% of the phenotypic variation in height, and we estimate that unidentified common variants of similar effect sizes would increase this figure to approximately 16% of phenotypic variation (approximately 20% of heritable variation). Although additional approaches are needed to dissect the genetic architecture of polygenic human traits fully, our findings indicate that GWA studies can identify large numbers of loci that implicate biologically relevant genes and pathways.

New insights into the genetic etiology of Alzheimer's disease and related dementias

Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/'proxy' AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele

Genome-wide association identifies nine common variants associated with fasting proinsulin levels and provides new insights into the pathophysiology of type 2 diabetes.

OBJECTIVE: Proinsulin is a precursor of mature insulin and C-peptide. Higher circulating proinsulin levels are associated with impaired β-cell function, raised glucose levels, insulin resistance, and type 2 diabetes (T2D). Studies of the insulin processing pathway could provide new insights about T2D pathophysiology. RESEARCH DESIGN AND METHODS: We have conducted a meta-analysis of genome-wide association tests of ∼2.5 million genotyped or imputed single nucleotide polymorphisms (SNPs) and fasting proinsulin levels in 10,701 nondiabetic adults of European ancestry, with follow-up of 23 loci in up to 16,378 individuals, using additive genetic models adjusted for age, sex, fasting insulin, and study-specific covariates. RESULTS: Nine SNPs at eight loci were associated with proinsulin levels (P < 5 × 10(-8)). Two loci (LARP6 and SGSM2) have not been previously related to metabolic traits, one (MADD) has been associated with fasting glucose, one (PCSK1) has been implicated in obesity, and four (TCF7L2, SLC30A8, VPS13C/C2CD4A/B, and ARAP1, formerly CENTD2) increase T2D risk. The proinsulin-raising allele of ARAP1 was associated with a lower fasting glucose (P = 1.7 × 10(-4)), improved β-cell function (P = 1.1 × 10(-5)), and lower risk of T2D (odds ratio 0.88; P = 7.8 × 10(-6)). Notably, PCSK1 encodes the protein prohormone convertase 1/3, the first enzyme in the insulin processing pathway. A genotype score composed of the nine proinsulin-raising alleles was not associated with coronary disease in two large case-control datasets. CONCLUSIONS: We have identified nine genetic variants associated with fasting proinsulin. Our findings illuminate the biology underlying glucose homeostasis and T2D development in humans and argue against a direct role of proinsulin in coronary artery disease pathogenesis

Rare coding variants in PLCG2, ABI3, and TREM2 implicate microglial-mediated innate immunity in Alzheimer's disease

We identified rare coding variants associated with Alzheimer’s disease (AD) in a 3-stage case-control study of 85,133 subjects. In stage 1, 34,174 samples were genotyped using a whole-exome microarray. In stage 2, we tested associated variants (P<1×10-4) in 35,962 independent samples using de novo genotyping and imputed genotypes. In stage 3, an additional 14,997 samples were used to test the most significant stage 2 associations (P<5×10-8) using imputed genotypes. We observed 3 novel genome-wide significant (GWS) AD associated non-synonymous variants; a protective variant in PLCG2 (rs72824905/p.P522R, P=5.38×10-10, OR=0.68, MAFcases=0.0059, MAFcontrols=0.0093), a risk variant in ABI3 (rs616338/p.S209F, P=4.56×10-10, OR=1.43, MAFcases=0.011, MAFcontrols=0.008), and a novel GWS variant in TREM2 (rs143332484/p.R62H, P=1.55×10-14, OR=1.67, MAFcases=0.0143, MAFcontrols=0.0089), a known AD susceptibility gene. These protein-coding changes are in genes highly expressed in microglia and highlight an immune-related protein-protein interaction network enriched for previously identified AD risk genes. These genetic findings provide additional evidence that the microglia-mediated innate immune response contributes directly to AD development