Competition among native and invasive Phragmites australis populations: An experimental test of the effects of invasion status, genome size, and ploidy level

Among the traits whose relevance for plant invasions has recently been suggested are genome size (the amount of nuclear DNA) and ploidy level. So far, research on the role of genome size in invasiveness has been mostly based on indirect evidence by comparing species with different genome sizes, but how karyological traits influence competition at the intraspecific level remains unknown. We addressed these questions in a common-garden experiment evaluating the outcome of direct intraspecific competition among 20 populations of Phragmites australis, represented by clones collected in North America and Europe, and differing in their status (native and invasive), genome size (small and large), and ploidy levels (tetraploid, hexaploid, or octoploid). Each clone was planted in competition with one of the others in all possible combinations with three replicates in 45-L pots. Upon harvest, the identity of 21 shoots sampled per pot was revealed by flow cytometry and DNA analysis. Differences in performance were examined using relative proportions of shoots of each clone, ratios of their aboveground biomass, and relative yield total (RYT). The performance of the clones in competition primarily depended on the clone status (native vs. invasive). Measured in terms of shoot number or aboveground biomass, the strongest signal observed was that North American native clones always lost in competition to the other two groups. In addition, North American native clones were suppressed by European natives to a similar degree as by North American invasives. North American invasive clones had the largest average shoot biomass, but only by a limited, nonsignificant difference due to genome size. There was no effect of ploidy on competition. Since the North American invaders of European origin are able to outcompete the native North American clones, we suggest that their high competitiveness acts as an important driver in the early stages of their invasion

Chapter 2. Trends and status of alien and invasive alien species

Chapter 2: Trends and status of alien and invasive alien species of the Thematic Assessment Report on Invasive Alien Species and their Control of the Intergovernmental Science-Policy Platform on Biodiversity and Ecosystem Services

An Integrated TCGA Pan-Cancer Clinical Data Resource to Drive High-Quality Survival Outcome Analytics

For a decade, The Cancer Genome Atlas (TCGA) program collected clinicopathologic annotation data along with multi-platform molecular profiles of more than 11,000 human tumors across 33 different cancer types. TCGA clinical data contain key features representing the democratized nature of the data collection process. To ensure proper use of this large clinical dataset associated with genomic features, we developed a standardized dataset named the TCGA Pan-Cancer Clinical Data Resource (TCGA-CDR), which includes four major clinical outcome endpoints. In addition to detailing major challenges and statistical limitations encountered during the effort of integrating the acquired clinical data, we present a summary that includes endpoint usage recommendations for each cancer type. These TCGA-CDR findings appear to be consistent with cancer genomics studies independent of the TCGA effort and provide opportunities for investigating cancer biology using clinical correlates at an unprecedented scale. Analysis of clinicopathologic annotations for over 11,000 cancer patients in the TCGA program leads to the generation of TCGA Clinical Data Resource, which provides recommendations of clinical outcome endpoint usage for 33 cancer types

Invasion syndromes: a systematic approach for predicting biological invasions and facilitating effective management

Published: 02 March 2020Our ability to predict invasions has been hindered by the seemingly idiosyncratic context-dependency of individual invasions. However, we argue that robust and useful generalisations in invasion science can be made by considering “invasion syndromes” which we define as “a combination of pathways, alien species traits, and characteristics of the recipient ecosystem which collectively result in predictable dynamics and impacts, and that can be managed effectively using specific policy and management actions”. We describe this approach and outline examples that highlight its utility, including: cacti with clonal fragmentation in arid ecosystems; small aquatic organisms introduced through ballast water in harbours; large ranid frogs with frequent secondary transfers; piscivorous freshwater fishes in connected aquatic ecosystems; plant invasions in high-elevation areas; tall-statured grasses; and tree-feeding insects in forests with suitable hosts. We propose a systematic method for identifying and delimiting invasion syndromes. We argue that invasion syndromes can account for the context-dependency of biological invasions while incorporating insights from comparative studies. Adopting this approach will help to structure thinking, identify transferrable risk assessment and management lessons, and highlight similarities among events that were previously considered disparate invasion phenomena.Ana Novoa, David M. Richardson, Petr Pyšek, Laura A. Meyerson, Sven Bacher ... Jasmin Packer ... et al

Driver Fusions and Their Implications in the Development and Treatment of Human Cancers.

Gene fusions represent an important class of somatic alterations in cancer. We systematically investigated fusions in 9,624 tumors across 33 cancer types using multiple fusion calling tools. We identified a total of 25,664 fusions, with a 63% validation rate. Integration of gene expression, copy number, and fusion annotation data revealed that fusions involving oncogenes tend to exhibit increased expression, whereas fusions involving tumor suppressors have the opposite effect. For fusions involving kinases, we found 1,275 with an intact kinase domain, the proportion of which varied significantly across cancer types. Our study suggests that fusions drive the development of 16.5% of cancer cases and function as the sole driver in more than 1% of them. Finally, we identified druggable fusions involving genes such as TMPRSS2, RET, FGFR3, ALK, and ESR1 in 6.0% of cases, and we predicted immunogenic peptides, suggesting that fusions may provide leads for targeted drug and immune therapy

What Do Community Benefits Agreements Deliver? Evidence From Los Angeles

Problem, research strategy, and findings: Advocates of community benefits agreements (CBAs) between coalitions of nongovernmental organizations (NGOs) and real estate developers contend that CBAs promote public accountability and responsiveness to community concerns. This study assesses the Los Angeles Sports and Entertainment District (LASED) CBA, which scholars and practitioners have described as a model for such agreements. I assess compliance with key provisions of the agreement related to jobs, affordable housing, and parks and recreational facilities. I also assess whether compliance with these provisions has yielded benefits beyond those required under existing laws and regulations. I find that the parties to the agreement have technically complied with many, although arguably not all, of its provisions. But some of the provisions in the CBA are not legally binding, other provisions overlap with requirements that the developer would have had to satisfy even without the CBA, and some reports required by the CBA are unavailable. As a result, outcomes such as living wage jobs and funding for affordable housing units are not clearly attributable to the CBA; other outcomes, such as targeted hiring, are unknown due to a lack of relevant information.Takeaway for practice: Although CBAs may not fulfill all the claims that advocates make on their behalf, they can play important roles in community development by directing public and private spending to underserved neighborhoods. But collecting and verifying the relevant data may be challenging, even if reporting requirements are clearly spelled out in the CBA. As the complexity of a CBA increases, so do the challenges of assessing outcomes and assigning responsibility for those outcomes

Genomic and Functional Approaches to Understanding Cancer Aneuploidy

Aneuploidy, whole chromosome or chromosome arm imbalance, is a near-universal characteristic of human cancers. In 10,522 cancer genomes from The Cancer Genome Atlas, aneuploidy was correlated with TP53 mutation, somatic mutation rate, and expression of proliferation genes. Aneuploidy was anti-correlated with expression of immune signaling genes, due to decreased leukocyte infiltrates in high-aneuploidy samples. Chromosome arm-level alterations show cancer-specific patterns, including loss of chromosome arm 3p in squamous cancers. We applied genome engineering to delete 3p in lung cells, causing decreased proliferation rescued in part by chromosome 3 duplication. This study defines genomic and phenotypic correlates of cancer aneuploidy and provides an experimental approach to study chromosome arm aneuploidy. Analyzing >10,000 human cancers, Taylor et al. show that aneuploidy is correlated with somatic mutation rate, expression of proliferation genes, and decreased leukocyte infiltration. Loss of chromosome arm 3p is common in squamous cancers, but deletion of chromosome 3p reduces cell proliferation in vitro

Oncogenic Signaling Pathways in The Cancer Genome Atlas

Genetic alterations in signaling pathways that control cell-cycle progression, apoptosis, and cell growth are common hallmarks of cancer, but the extent, mechanisms, and co-occurrence of alterations in these pathways differ between individual tumors and tumor types. Using mutations, copy-number changes, mRNA expression, gene fusions and DNA methylation in 9,125 tumors profiled by The Cancer Genome Atlas (TCGA), we analyzed the mechanisms and patterns of somatic alterations in ten canonical pathways: cell cycle, Hippo, Myc, Notch, Nrf2, PI-3-Kinase/Akt, RTK-RAS, TGFb signaling, p53 and beta-catenin/Wnt. We charted the detailed landscape of pathway alterations in 33 cancer types, stratified into 64 subtypes, and identified patterns of co-occurrence and mutual exclusivity. Eighty-nine percent of tumors had at least one driver alteration in these one alteration potentially targetable by currently available drugs. Thirty percent of tumors had multiple targetable alterations, indicating opportunities for combination therapy