Fagus sylvatica seedlings show provenance differentiation rather than adaptation to soil in a transplant experiment.

BACKGROUND: Understanding and predicting the response of tree populations to climate change requires understanding the pattern and scale of their adaptation. Climate is often considered the major driver of local adaptation but, although biotic factors such as soil pathogens or mutualists could be as important, their role has typically been neglected. Biotic drivers might also interact with climate to affect performance and mycorrhizae, in particular, are likely to play a key role in determining drought resistance, which is important in the context of adaptation to future environmental change. To address these questions, we performed a fully reciprocal soil-plant transplant experiment using Fagus sylvatica seedlings and soils from three regions in Germany. To separate the biotic and abiotic effects of inoculation, half of the plants were inoculated with natural soil from the different origins, while the rest were grown on sterilized substrate. We also imposed a drought stress treatment to test for interactions between soil biota and climate. After 1 year of growth, we measured aboveground biomass of all seedlings, and quantified mycorrhizal colonization for a subset of the seedlings, which included all soil-plant combinations, to disentangle the effect of mycorrhiza from other agents. RESULTS: We found that plant origin had the strongest effect on plant performance, but this interacted with soil origin. In general, trees showed a slight tendency to produce less aboveground biomass on local soils, suggesting soil antagonists could be causing trees to be maladapted to their local soils. Consistently, we found lower mycorrhizal colonization rate under local soil conditions. Across all soils, seedlings from low elevations produced more annual biomass than middle (+ 290%) and high (+ 97%) elevations. Interestingly, mycorrhizal colonization increased with drought in the two provenances that showed higher drought tolerance, which supports previous results showing that mycorrhizae can increase drought resistance. CONCLUSIONS: Our findings suggest that soil communities play a role in affecting early performance of temperate trees, although this role may be smaller than that of seed origin. Also, other effects, such as the positive response to generalists or negative interactions with soil biota may be as important as the highly specialized mycorrhizal associations.

Light-dependent growth rate determines changes in the population of Planktothrix rubescens over the annual cycle in Lake Zürich, Switzerland.

• Analyses were made to determine which changes in a Lake Zürich population of Planktothrix rubescens were dependent on light- and temperature-dependent growth rates, and when growth was limited by the mixing depth. • Changes in vertical distribution of the cyanobacterium, determined weekly from August 1998 to September 1999, were related to growth increments calculated at 1-h time and 1-m depth intervals from values of irradiance, attenuance, temperature and biomass in the lake, using algorithms based on growth rates in culture. • Population biovolume varied annually from 1.2 to 120  cm3  m-2 . During summer, modelled growth in the metalimnion matched the 50-fold population increase. Modelled growth exceeded the observed increase when Planktothrix was mixed into the nutrient-depleted epilimnion, suggesting nutrient limitation. The measured increase ceased when the mixed depth exceeded the critical depth for growth in autumn (Sverdrup's principle). Light limitation explained the gradual decrease of the population in winter. The steep decline in spring had other causes. • Population changes were largely determined by interactions of light and depth distribution; decreases in nutrient loading have had little impact on Planktothrix growth in Lake Zürich.

p53-dependent cell cycle arrest induced by N-acetyl-L-leucinyl-L-leucinyl-L-norleucinal in platelet-derived growth factor-stimulated human fibroblasts.

Proteases are known to play important roles in cell growth control, although the underlying mechanisms are still poorly understood. Here we show that the protease inhibitor N-acetyl-L-leucinyl-L-leucinyl-L-norleucinal induced cell cycle arrest in platelet-derived growth factor-stimulated human fibroblasts at the G1/S boundary of the cell cycle by inhibiting the proteasome. Inhibition of the proteasome resulted in accumulation of the tumor suppressor p53, which was followed by an increase in the amount of the cyclin-dependent kinase-inhibitor p21. As a consequence, both phosphorylation and activity of the cyclin-dependent kinase 2/cyclin E complex were inhibited. We further observed that the retinoblastoma gene product, pRb, remained in the hypophosphorylated state, thus preventing cells from progression into the S-phase. These studies strongly support the hypothesis that the proteasome is a key regulator in the G1-phase of cell cycle progression.

[Effect of calcium antagonists (nifedipine) on nephrocalcinosis and calcium excretion in the rat]. / Zur Wirkung von Kalziumantagonisten (Nifedipin) auf die Nephrokalzinose und Kalziumausscheidung der Ratte.

An animal model was established to test the effect of a calcium antagonist on nephrocalcinosis, which was induced by an atherogenous diet, and its effect on the excretion of calcium and other parameters relevant for stone formation. With the administration of nifedipine (Adalat), the grade of nephrocalcinosis could be significantly reduced. Furthermore, with nifedipine the excretion of calcium and sodium in the urine was raised, while phosphate and potassium levels were lowered. The excretion of magnesium and citrate, reduced by an atherogenous diet, could be raised significantly with the administration of nifedipine. The pathophysiological mechanisms underlying the effect of nifedipine on nephrocalcinosis and on the excretion of the urine parameters are discussed. Apparently hypercalciuria is the result of a reduced reabsorption of calcium in the tubulus. The inhibitory effect on the genesis of nephrocalcinosis is possibly due to the lower calcium influx into the tubular cells.