40 research outputs found

    Disease decreases variation in host community structure in an old-field grassland

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    Disease may drive variation in host community structure by modifying the interplay of deterministic and stochastic processes that shape communities. For instance, deterministic processes like ecological selection can benefit species less impacted by disease. When communities have higher levels of disease and disease consistently selects for certain host species, this can reduce variation in host community composition. On the other hand, when host communities are less impacted by disease and selection is weaker, stochastic processes (e.g., drift, dispersal) may play a bigger role in host community structure, which can increase variation among communities. While effects of disease on host community structure have been quantified in field experiments, few have addressed the role of disease in modulating variation in structure among host communities. To address this, we conducted a field experiment spanning three years, using a tractable system: foliar fungal pathogens in an old-field grassland community dominated by the grass Lolium arundinaceum, tall fescue. We reduced foliar fungal disease burden in replicate host communities (experimental plots in intact vegetation) in three fungicide regimens that varied in the seasonal duration of fungicide treatment and included a fungicide-free control. We measured host diversity, biomass, and variation in community structure among replicate communities. Disease reduction generally decreased plant richness and increased aboveground biomass relative to communities experiencing ambient levels of disease. These changes in richness and aboveground biomass were consistent across years despite changes in structure of the plant communities over the experiment’s three years. Importantly, disease reduction amplified host community variation, suggesting that disease diminished the degree to which host communities were structured by stochastic processes. These results of experimental disease reduction both highlight the potential importance of stochastic processes in plant communities and reveal the potential for disease to regulate variation in host community structure

    Burning questions for a warming and changing world: 15 unknowns in plant abiotic stress

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    We present unresolved questions in plant abiotic stress biology as posed by 15 research groups with expertise spanning eco-physiology to cell and molecular biology. Common themes of these questions include the need to better understand how plants detect water availability, temperature, salinity, and rising carbon dioxide (CO2) levels; how environmental signals interface with endogenous signaling and development (e.g. circadian clock and flowering time); and how this integrated signaling controls downstream responses (e.g. stomatal regulation, proline metabolism, and growth versus defense balance). The plasma membrane comes up frequently as a site of key signaling and transport events (e.g. mechanosensing and lipid-derived signaling, aquaporins). Adaptation to water extremes and rising CO2 affects hydraulic architecture and transpiration, as well as root and shoot growth and morphology, in ways not fully understood. Environmental adaptation involves tradeoffs that limit ecological distribution and crop resilience in the face of changing and increasingly unpredictable environments. Exploration of plant diversity within and among species can help us know which of these tradeoffs represent fundamental limits and which ones can be circumvented by bringing new trait combinations together. Better defining what constitutes beneficial stress resistance in different contexts and making connections between genes and phenotypes, and between laboratory and field observations, are overarching challenges.Paul E. Verslues ... Stephen D. Tyerman ... et al

    ANOMALOUS REACTION MEAN FREE PATHS OF NUCLEAR PROJECTILE FRAGMENTS FROM HEAVY ION COLLISIONS AT 2 AGeV

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    We present in detail the description and the analysis of two independent experiments using Bevalac beams of {sup 16}O and {sup 56}Fe. From their results it is concluded that the reaction mean free paths of relativistic projectile fragments, 3 {<=} Z {<=} 26, are shorter for a few centimeters after emission than at large distances where they are compatible with values predicted from experiments on beam nuclei. The probability that this effect is due to a statistical fluctuation is <10{sup -3}. The effect is enhanced in later generations of fragments, the correlation between successive generations suggesting a kind of "memory" for the anomaly. Various systematic and spurious effects as well as conventional explanations are discussed mainly on the basis of direct experimental observations internal to our data, and found not to explain our results. The data can be interpreted by the relatively rare occurrence of anomalous fragments that interact with an unexpectedly large cross section. The statistical methods used in the analysis of the observations are fully described
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