Aim: Forecasting species migration with climate change and the advance of biological invasions requires a better understanding of species' relative migration capacity. Although theory predicts that species combining high fecundity and dispersal with early maturation should spread the fastest, possible correlations between these traits greatly complicate predictions of species' relative spread velocity. We asked whether the demographic and dispersal rates controlling plant population spread are correlated across species, and which observed association of these traits leads to the fastest spread. Location: Worldwide. Time period: Current. Major taxa studied: Eighty species of herbaceous and woody plants from 35 families and 64 genera. Methods: We examined the relationships between age at maturity, dispersal and fecundity for 80 plant species, ranging from annual herbs to trees. We incorporated these rates into a model predicting spread velocities, in order to estimate species' spread capacity as a function of their life history. Results: Across species, age at maturity was positively associated with both dispersal and fecundity. Given that these traits have opposing effects on spread, our models predict that species widely spaced along an age-at-maturity gradient should spread at comparable rates. This result was driven by variation between rather than within life-forms; the traits controlling spread were not correlated within annual herbs, perennial herbs or trees. The predicted spread velocities for these plant life-forms overlapped considerably, although on average, trees were predicted to spread faster than herbaceous species. Main conclusions: Our results suggest that very different plant life histories allow for similar rates of biological invasion or native species migration under climate change. Determining where species fall within the correlated suite of traits controlling spread might provide the most effective way to predict relative spread velocities.

Biological invasions severely impact native plant communities, causing dramatic shifts in species composition and the restriction of native species to spatially isolated refuges. Competition from resident species and the interaction between resource limitation and competition have been overlooked as mechanisms of community resistance in refugia habitats. We examined the importance of these factors in determining the resistance of California serpentine plant communities to invasion by three common European grasses, Avena barbata, Bromus diandrus, and Hordeum murinum. We added seeds of each of these grasses to plots subjected to six levels of resource addition (N, P, Ca, H2O, all resources together, and a no-addition control) and two levels of competition (with resident community present or removed). Resource limitation and competition had strong effects on the biomass and reproduction of the three invaders. The addition of all resources together combined with the removal of the resident community yielded individual plants that were fourfold to 20-fold larger and sixfold to 20-fold more fecund than plants from control plots. Competitor removal alone yielded invaders that were twofold to sevenfold larger and twofold to ninefold more fecund. N addition alone or in combination with other resources led to a twofold to ninefold increase in the biomass and fecundity of the invaders. No other resource alone significantly affected native or invader performance, suggesting that N was the key limiting resource during our experiment. We found a significant interaction between abiotic and biotic resistance for Bromus, which experienced increased competitive suppression in fertilized plots. The threefold increase in resident biomass with N addition was likely responsible for this result. Our results confirm that serpentine plant communities are severely N limited, which, in combination with competition from resident species, promotes the resistance of these systems to invasions. Our work suggests that better understanding the relative sensitivities of invaders and residents to the physical environment is critical to predicting how abiotic and biotic factors interact to determine community resistance.

Predicting the speed of biological invasions and native species migrations requires an understanding of the ecological and evolutionary dynamics of spreading populations. Theory predicts that evolution can accelerate species’ spread velocity, but how landscape patchiness—an important control over traits under selection—influences this process is unknown. We manipulated the response to selection in populations of a model plant species spreading through replicated experimental landscapes of varying patchiness. After six generations of change, evolving populations spread 11% farther than nonevolving populations in continuously favorable landscapes and 200% farther in the most fragmented landscapes. The greater effect of evolution on spread in patchier landscapes was consistent with the evolution of dispersal and competitive ability. Accounting for evolutionary change may be critical when predicting the velocity of range expansions.

Gene flow between populations may either support local adaptation by supplying genetic variation on which selection may act, or counteract it if maladapted alleles arrive faster than can be purged by selection. Although both such effects have been documented within plant species' native ranges, how the balance of these forces influences local adaptation in invasive plant populations is less clear, in part because introduced species often have lower genetic variation initially but also tend to have good dispersal abilities. To evaluate the extent of gene flow and adaptation to local climate in invasive populations of Solidago canadensis, and the implications of this for range expansion, we compared population differentiation at microsatellite and chloroplast loci for populations across Switzerland and assessed the effect of environmental transfer distance using common gardens. We found that while patterns of differentiation at neutral genetic markers suggested that populations are connected through extensive pollen and seed movement, common-garden plants nonetheless exhibited modest adaptation to local climate conditions. Growth rate and flower production declined with climatic distance from a plant's home site, with clones from colder home sites performing better at or above the range limit. Such adaptation in invasive species is likely to promote further spread, particularly under climate change, as the genotypes positioned near the range edge may be best able to take advantage of lengthening growing seasons to expand the range.

On September 14-15, 2015, a meeting of clinicians and investigators in the fields of veterinary and human neuro-oncology, clinical trials, neuropathology, and drug development was convened at the National Institutes of Health campus in Bethesda, Maryland. This meeting served as the inaugural event launching a new consortium focused on improving the knowledge, development of, and access to naturally occurring canine brain cancer, specifically glioma, as a model for human disease. Within the meeting, a SWOT (strengths, weaknesses, opportunities, and threats) assessment was undertaken to critically evaluate the role that naturally occurring canine brain tumors could have in advancing this aspect of comparative oncology aimed at improving outcomes for dogs and human beings. A summary of this meeting and subsequent discussion are provided to inform the scientific and clinical community of the potential for this initiative. Canine and human comparisons represent an unprecedented opportunity to complement conventional brain tumor research paradigms, addressing a devastating disease for which innovative diagnostic and treatment strategies are clearly needed.

Sporadic gliomas in companion dogs provide a window on the interaction between tumorigenic mechanisms and host environment. We compared the molecular profiles of canine gliomas with those of human pediatric and adult gliomas to characterize evolutionarily conserved mammalian mutational processes in gliomagenesis. Employing whole-genome, exome, transcriptome, and methylation sequencing of 83 canine gliomas, we found alterations shared between canine and human gliomas such as the receptor tyrosine kinases, TP53 and cell-cycle pathways, and IDH1 R132. Canine gliomas showed high similarity with human pediatric gliomas per robust aneuploidy, mutational rates, relative timing of mutations, and DNA-methylation patterns. Our cross-species comparative genomic analysis provides unique insights into glioma etiology and the chronology of glioma-causing somatic alterations.