Declining biodiversity represents one of the most dramatic and irreversible aspects of anthropogenic global change, yet the ecological implications of this change are poorly understood. Recent studies have shown that biodiversity loss of basal species, such as autotrophs or plants, affects fundamental ecosystem processes such as nutrient dynamics and autotrophic production. Ecological theory predicts that changes induced by the loss of biodiversity at the base of an ecosystem should impact the entire system. Here we show that experimental reductions in grassland plant richness increase ecosystem vulnerability to invasions by plant species, enhance the spread of plant fungal diseases, and alter the richness and structure of insect communities. These results suggest that the loss of basal species may have profound effects on the integrity and functioning of ecosystems.
In an experiment that directly manipulated grassland plant species richness and composition, decreased plant species richness (“diversity”) increased pathogen load (the percentage of leaf area infected by species‐specific foliar pathogens across the plant community) in 1998. Pathogen load was almost three times greater in the average monoculture than in the average plot planted with 24 grassland plant species, an approximately natural diversity. Eleven individual diseases increased in severity (percentage of leaf area infected by a single disease) at lower plant species richness, and severity of only one disease was positively correlated with diversity. For 10 of the 11 diseases whose severity was negatively related to diversity, disease severity was positively correlated with host abundance, and in six of these cases, species diversity had no effect on disease severity after controlling for the effects of host abundance. These results suggest that increased abundances of individual host species at lower species diversity increased disease transmission and severity. In 1996 and 1997, similar results for a smaller number of diseases sampled were found in this experiment and another similar one. Although the effect of diversity on disease was highly significant, considerable variance in pathogen load remained among plots of a given diversity level. Much of this residual variance was explained by community characteristics that were a function of the species composition of the communities (the identity of species present vs. those lost). Specifically, communities that lost less disease‐prone species had higher pathogen loads; this effect explained more variance in pathogen load than did diversity. Also, communities that lost the species dominant at high diversity had higher pathogen loads, presumably because relaxed competition allowed greater increases in host abundances, but this effect was weak. Among plant species, disease proneness appeared to be determined more by regional than local processes, because it was better correlated with frequency of the plant species' populations across the region than with local abundance or frequency across the state. In total, our results support the hypothesis that decreased species diversity will increase foliar pathogen load if this increases host abundance and, therefore, disease transmission. Additionally, changes in community characteristics determined by species composition will strongly influence pathogen load.
Three components of global change, elevated CO2, nitrogen addition, and decreased plant species richness (‘diversity’), increased the percent leaf area infected by fungi (pathogen load) for much to all of the plant community in one year of a factorial grassland experiment. Decreased plant diversity had the broadest effect, increasing pathogen load across the plant community. Decreased diversity increased pathogen load primarily by allowing remaining plant species to increase in abundance, facilitating spread of foliar fungal pathogens specific to each plant species. Changes in plant species composition also strongly influenced community pathogen load, with communities that lost less disease prone plant species increasing more in pathogen load. Elevated CO2 increased pathogen load of C3 grasses, perhaps by decreasing water stress, increasing leaf longevity, and increasing photosynthetic rate, all of which can promote foliar fungal disease. Decreased plant diversity further magnified the increase in C3 grass pathogen load under elevated CO2. Nitrogen addition increased pathogen load of C4 grasses by increasing foliar nitrogen concentration, which can enhance pathogen infection, growth, and reproduction. Because changes in foliar fungal pathogen load can strongly influence grassland ecosystem processes, our study suggests that increased pathogen load can be an important mechanism by which global change affects grassland ecosystems.
Breeders of hard red spring wheat (Triticum aestivum) are attempting to incorporate resistance to scab, caused by Fusarium graminearum. In artificially inoculated, replicated field plots, 37 wheat entries (inbred lines or cultivars) were evaluated for 3 years and an additional 60 entries for 2 of the 3 years for incidence (percent spikes infected), severity (percent infected spikelets within infected spikes), and disease index (percent infected spikelets in 50-spike sample). From year to year, entries had similar index values, with coefficients of determination (r 2) ranging from 0.59 to 0.78, with a mean of 0.73. Entries appeared slightly more similar from year to year for incidence than for severity, although both measures of disease had highly significant r 2 values. Incidence and severity were highly correlated in the wheat germ plasm examined; r 2 values in single years ranged from 0.51 to 0.67, with a mean of 0.64. A representative subset of 22 entries was included for a fourth year. None of the measures of disease in year 4 correlated with their counterparts in any of the first 3 years. This loss of repeatability may have been caused by severe lodging or by high temperatures during the evaluation period that accelerated disease progress and wheat maturity during year 4. Incidence and severity remained correlated in year 4 (r 2 = 0.60).
ROELFS, A. P., and J. V. GROTH. 1980. A comparison of virulence phenotypes in wheat stem rust populations reproducing sexually and asexually.Phytopathology 70:855-862.The number and distribution of 16 loci expressing virulence were loci expressing virulence per isolate was about 6 and 10 for the sexual and compared in two populations of wheat stem rust in the USA. In 1975, asexual populations, respectively. The distribution of numbers of loci samples were collected from a population on barley and wheat in Idaho and expressing virulence differences between pairs of isolates was nearly Washington that undergoes sexual reproduction annually and from a random in the sexual population, while it was characterized by clusters of population east of the Rocky Mountains that reproduces asexually.phenotypes in the asexual population. These clusters differed from one Virulence was determined by inoculating 16 wheat lines, each differing by a another by 4 to 10 genes expressing virulence; genotypes within clusters single gene for stem rust resistance. The sexual population had a larger differed by 1 to 2 loci. None of the loci, examined in all of their paired frequency of distinct phenotypes expressed as a percentage. In the sexual combinations, deviated strongly from expected mean frequencies based on population, the frequency was 23.5% with 426 isolates and in the asexual products of individual locus frequencies, providing no evidence for strong population it was 0.07% with 2,377 isolates. Simpson's measure of diversity positive or negative fitness effects associated with individual genes. was 0.974 and 0.501 for the two populations, respectively. Mean number of
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