The reliability of observational approaches for detecting interspecific parasite interactions:comparison with experimental results

Interactions among coinfecting parasites have the potential to alter host susceptibility to infection, the progression of disease and the efficacy of disease control measures. It is therefore essential to be able to accurately infer the occurrence and direction of such interactions from parasitological data. Due to logistical constraints, perturbation experiments are rarely undertaken to directly detect interactions, therefore a variety of approaches are commonly used to infer them from patterns of parasite association in observational data. However, the reliability of these various approaches is not known. We assess the ability of a range of standard analytical approaches to detect known interactions between infections of nematodes and intestinal coccidia (Eimeria) in natural small-mammal populations, as revealed by experimental perturbations. We show that correlation-based approaches are highly unreliable, often predicting strong and highly significant associations between nematodes and Eimeria in the opposite direction to the underlying interaction. The most reliable methods involved longitudinal analyses, in which the nematode infection status of individuals at one month is related to the infection status by Eimeria the next month. Even then, however, we suggest these approaches are only viable for certain types of infections and datasets. Overall we suggest that, in the absence of experimental approaches, careful consideration be given to the choice of statistical approach when attempting to infer interspecific interactions from observational data

Enhanced weathering in the U.S. Corn Belt delivers carbon removal with agronomic benefits

Enhanced weathering (EW) with crushed basalt on farmlands is a promising scalable atmospheric carbon dioxide removal strategy that urgently requires performance assessment with commercial farming practices. Our large-scale replicated EW field trial in the heart of the U.S. Corn Belt shows cumulative time-integrated carbon sequestration of 15.4 +/- 4.1 t CO2 ha-1 over four years, with additional emissions mitigation of ~0.1 - 0.4 t CO2,e ha-1 yr-1 for soil nitrous oxide, a potent long-lived greenhouse gas. Maize and soybean yields increased 12-16% with EW following improved soil fertility, decreased soil acidification, and upregulation of root nutrient transport genes. Our findings suggest that widespread adoption of EW across farming sectors has the potential to contribute significantly to net-zero greenhouse gas emissions goals and global food and soil security

Bringing It All Together: Multi-species Integrated Population Modelling of a Breeding Community

Integrated population models (IPMs) combine data on different aspects of demography with time-series of population abundance. IPMs are becoming increasingly popular in the study of wildlife populations, but their application has largely been restricted to the analysis of single species. However, species exist within communities: sympatric species are exposed to the same abiotic environment, which may generate synchrony in the fluctuations of their demographic parameters over time. Given that in many environments conditions are changing rapidly, assessing whether species show similar demographic and population responses is fundamental to quantifying interspecific differences in environmental sensitivity and highlighting ecological interactions at risk of disruption. In this paper, we combine statistical approaches to study populations, integrating data along two different dimensions: across species (using a recently proposed framework to quantify multi-species synchrony in demography) and within each species (using IPMs with demographic and abundance data).We analyse data from three seabird species breeding at a nationally important long-term monitoring site. We combine demographic datasets with island-wide population counts to construct the first multi-species Integrated Population Model to consider synchrony. Our extension of the IPM concept allows the simultaneous estimation of demographic parameters, adult abundance and multi-species synchrony in survival and productivity, within a robust statistical framework. The approach is readily applicable to other taxa and habitats

Pathogenic mutation in the ALS/FTD gene, CCNF, causes elevated Lys48-linked ubiquitylation and defective autophagy

Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are fatal neurodegenerative disorders that have common molecular and pathogenic characteristics, such as aberrant accumulation and ubiquitylation of TDP-43; however, the mechanisms that drive this process remain poorly understood. We have recently identified CCNF mutations in familial and sporadic ALS and FTD patients. CCNF encodes cyclin F, a component of an E3 ubiquitin–protein ligase (SCF) complex that is responsible for ubiquitylating proteins for degradation by the ubiquitin–proteasome system. In this study, we examined the ALS/FTD-causing p.Ser621Gly (p.S621G) mutation in cyclin F and its effect upon downstream Lys48-specific ubiquitylation in transfected Neuro-2A and SH-SY5Y cells. Expression of mutant cyclin F caused increased Lys48-specific ubiquitylation of proteins in neuronal cells compared to cyclin F. Proteomic analysis of immunoprecipitated Lys48-ubiquitylated proteins from mutant cyclin F-expressing cells identified proteins that clustered within the autophagy pathway, including sequestosome-1 (p62/SQSTM1), heat shock proteins, and chaperonin complex components. Examination of autophagy markers p62, LC3, and lysosome-associated membrane protein 2 (Lamp2) in cells expressing mutant cyclin F revealed defects in the autophagy pathway specifically resulting in impairment in autophagosomal–lysosome fusion. This finding highlights a potential mechanism by which cyclin F interacts with p62, the receptor responsible for transporting ubiquitylated substrates for autophagic degradation. These findings demonstrate that ALS/FTD-causing mutant cyclin F disrupts Lys48-specific ubiquitylation, leading to accumulation of substrates and defects in the autophagic machinery. This study also demonstrates that a single missense mutation in cyclin F causes hyper-ubiquitylation of proteins that can indirectly impair the autophagy degradation pathway, which is implicated in ALS pathogenesis

Agricultural weed research: a critique and two proposals

Two broad aims drive weed science research: improved management and improved understanding of weed biology and ecology. In recent years, agricultural weed research addressing these two aims has effectively split into separate subdisciplines despite repeated calls for greater integration. Although some excellent work is being done, agricultural weed research has developed a very high level of repetitiveness, a preponderance of purely descriptive studies, and has failed to clearly articulate novel hypotheses linked to established bodies of ecological and evolutionary theory. In contrast, invasive plant research attracts a diverse cadre of nonweed scientists using invasions to explore broader and more integrated biological questions grounded in theory. We propose that although studies focused on weed management remain vitally important, agricultural weed research would benefit from deeper theoretical justification, a broader vision, and increased collaboration across diverse disciplines. To initiate change in this direction, we call for more emphasis on interdisciplinary training for weed scientists, and for focused workshops and working groups to develop specific areas of research and promote interactions among weed scientists and with the wider scientific community.Fil: Ward, Sarah M. . State University Of Colorado - Fort Collins; Estados UnidosFil: Cousens, Roger D.. The University Of Melbourne; AustraliaFil: Bagavathiannan, Muthukumar V.. Texas A&M University; Estados UnidosFil: Barney, Jacob N.. Virginia Tech University; Estados UnidosFil: Beckie, Hugh J.. Agriculture and Agri-Food Canada; CanadáFil: Busi, Roberto. University of Western Australia; AustraliaFil: Davis, Adam S.. University Of Illinois; Estados UnidosFil: Dukes, Jeffrey S.. Purdue University; Estados UnidosFil: Forcella, Frank.Fil: Freckleton, Robert P.. University of Sheffield; Reino UnidoFil: Gallandt, Eric R.. University of Maine; Estados UnidosFil: Hall, Linda M.. University of Edmonton; CanadáFil: Jasieniuk, Marie. University of California; Estados UnidosFil: Lawton Rauh, Amy. Clemson University; Estados UnidosFil: Lehnhoff, Erik A.. Montana State University; Estados UnidosFil: Liebman, Matt. Iowa State University; Estados UnidosFil: Maxwell, Bruce D.. Montana State University; Estados UnidosFil: Mesgaran, Mohsen B.. The University Of Melbourne; AustraliaFil: Murray, Justine V.. CSIRO Ecosystem Sciences and Water for Healthy Country Flagship; AustraliaFil: Neve, Paul. Rothamsted Research; Reino UnidoFil: Nuñez, Martin Andres. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Patagonia Norte. Instituto de Investigación en Biodiversidad y Medioambiente; Argentina. Universidad Nacional del Comahue. Centro Regional Universitario Bariloche. Laboratorio de Ecotono; ArgentinaFil: Pauchard, Anibal. Universidad de Concepción; ChileFil: Queenborough, Simon A.. Ohio State University; Estados UnidosFil: Webber, Bruce L.. CSIRO Ecosystems Sciences; Australi

Genetic and immunopathological analysis of CHCHD10 in Australian amyotrophic lateral sclerosis and frontotemporal dementia and transgenic TDP-43 mice

Objective: Since the first report of CHCHD10 gene mutations in amyotrophiclateral sclerosis (ALS)/frontotemporaldementia (FTD) patients, genetic variation in CHCHD10 has been inconsistently linked to disease. A pathological assessment of the CHCHD10 protein in patient neuronal tissue also remains to be reported. We sought to characterise the genetic and pathological contribution of CHCHD10 to ALS/FTD in Australia. Methods: Whole-exome and whole-genome sequencing data from 81 familial and 635 sporadic ALS, and 108 sporadic FTD cases, were assessed for genetic variation in CHCHD10. CHCHD10 protein expression was characterised by immunohistochemistry, immunofluorescence and western blotting in control, ALS and/or FTD postmortem tissues and further in a transgenic mouse model of TAR DNA-binding protein 43 (TDP-43) pathology. Results: No causal, novel or disease-associated variants in CHCHD10 were identified in Australian ALS and/or FTD patients. In human brain and spinal cord tissues, CHCHD10 was specifically expressed in neurons. A significant decrease in CHCHD10 protein level was observed in ALS patient spinal cord and FTD patient frontal cortex. In a TDP-43 mouse model with a regulatable nuclear localisation signal (rNLS TDP-43 mouse), CHCHD10 protein levels were unaltered at disease onset and early in disease, but were significantly decreased in cortex in mid-stage disease. Conclusions: Genetic variation in CHCHD10 is not a common cause of ALS/FTD in Australia. However, we showed that in humans, CHCHD10 may play a neuron-specific role and a loss of CHCHD10 function may be linked to ALS and/or FTD. Our data from the rNLS TDP-43 transgenic mice suggest that a decrease in CHCHD10 levels is a late event in aberrant TDP-43-induced ALS/FTD pathogenesis

Are innovative species ecological generalists? A test in North American birds

Foraging innovation occurs when animals exploit novel food sources or invent new foraging techniques. Species vary widely in their rates of innovation, and these differences can be quantified using counts of novel behavior observed in the wild. One of the assumed benefits of innovativeness is that it allows species to exploit a wider variety of habitats and foods, enhancing survival when resources are in shortage or when individuals invade new environments. However, the relationship between innovation propensity and ecological generalism lacks firm empirical support. Moreover, innovativeness does not only imply benefits but may also lead to higher risks incurred in the wide array of habitats exploited. In this study, we test whether innovative species exploit a wider variety of habitats and food types as well as face the potential risk of more predators as a consequence of their ecological generalism. Using data for 193 North American bird species in a phylogenetically informed analysis, we find a significant positive relationship between innovation rate and habitat generalism, but not diet breadth. Although habitat generalism is also associated with exposure to a wider variety of predators, there is no direct relationship between innovation rate and predation. Our results suggest that although innovators use a wider variety of habitats, they are not necessarily diet generalists, challenging the classic view that feeding generalism is equivalent to feeding flexibility. Copyright 2011, Oxford University Press.