Refine
Has Fulltext
- no (4) (remove)
Document Type
- Article (4)
Language
- English (4)
Is part of the Bibliography
- yes (4)
Keywords
- calcium (4) (remove)
Institute
- Institut für Biochemie und Biologie (4) (remove)
Forest (or tree) age has been identified as an important determinant of the carbon (C) storage potential of forest soils. A large part of Central Europe's current forested area was affected by land use change with long periods of cultivation in past centuries suggesting that the organic C stocks in the soil (SOC) under recent forest may partly be legacies of the past and that stand age effects have to be distinguished from forest continuity effects (that is, the time since re-afforestation). We examined the influence of mean tree age and forest continuity on the SOC pool and the stores of total N and available P, Ca, Mg, and K in the soil (mineral soil and organic layer) across a sample of 14 beech (Fagus sylvatica) forests on sandy soil with variable tree age (23-189 years) and forest continuity (50-year-old afforestation to ancient ('permanent') forest, that is, > 230 years of proven continuity). Ancient beech forests (> 230 years of continuity) stored on average 47 and 44% more organic C and total N in the soil than recent beech afforestation (50-128 years of continuity). Contrary to expectation, we found large and significant C and N pool differences between the forest categories in the mineral soil but not in the organic layer indicating that decade- or century-long cultivation has reduced the subsoil C and nutrient stores while the organic layer element pools have approached a new equilibrium after only 50-128 years. PCA and correlation analyses suggest that forest continuity cannot be ignored when trying to understand the variation in soil C stocks between different stands. Forest clearing, subsequent cultivation, and eventual re-afforestation with beech resulted in similar relative stock reductions of C and N and, thus, no change in soil C/N ratio. We conclude that the continuity of forest cover, which may or may not be related to tree age, is a key determinant of the soil C and nutrient stores of beech forests in the old cultural landscape of Central Europe.
A 5-year old hunting dog was presented with reduced appetite, weight loss and polyuria/polydipsia. Hematology and clinical chemistry revealed anemia, leukocytosis, increased liver enzymes, hypoalbuminemia and hypercalcemia. The cytological, pathohistological and microbiological examination identified a disseminated infection with the saprophytic mould fungus Paecilomyces variotii in the biopsies of the spleen and a lymph node. Determination of vitamin D metabolites confirmed a calcitriol induced hypercalcemia.
Calcineurin is involved in development and cell differentiation of the social amoeba Dictyostelium discoideum. However, since knockouts of the calcineurin-encoding genes are not possible in D. discoideum it is assumed that the phosphatase also plays a crucial role during vegetative growth of the amoebae. Therefore, we investigated the role of calcineurin during vegetative growth in D. discoideum. RNAi-silenced calcineurin mutants showed cellular alterations with an abnormal morphology of mitochondria and had increased content of mitochondrial DNA (mtDNA). In contrast, mitochondria showed no substantial functional impairment. Calcineurin-silencing led to altered expression of calcium-regulated genes as well as mitochondrially-encoded genes. Furthermore, genes related to oxidative stress were higher expressed in the mutants, which correlated to an increased resistance towards reactive oxygen species (ROS). Most of the changes observed during vegetative growth were not seen after starvation of the calcineurin mutants. We show that impairment of calcineurin led to many subtle, but in the sum crucial cellular alterations in vegetative D. discoideum cells. As these alterations were not observed after starvation we propose a dual role for calcineurin during growth and development. Our results imply that calcineurin is one player in the mutual interplay between mitochondria and ROS during vegetative growth.
Bacterial pore-forming toxins compromise plasmalemmal integrity, leading to Ca2+ influx, leakage of the cytoplasm, and cell death. Such lesions can be repaired by microvesicular shedding or by the endocytic uptake of the injured membrane sites. Cells have at their disposal an entire toolbox of repair proteins for the identification and elimination of membrane lesions. Sphingomyelinases catalyze the breakdown of sphingomyelin into ceramide and phosphocholine. Sphingomyelin is predominantly localized in the outer leaflet, where it is hydrolyzed by acid sphingomyelinase (ASM) after lysosomal fusion with the plasma membrane. The magnesium-dependent neutral sphingomyelinase (NSM)-2 is found at the inner leaflet of the plasmalemma. Because either sphingomyelinase has been ascribed a role in the cellular stress response, we investigated their role in plasma membrane repair and cellular survival after treatment with the pore-forming toxins listeriolysin O (LLO) or pneumolysin (PLY). Jurkat T cells, in which ASM or NSM-2 was down-regulated [ASM knockdown (KD) or NSM-2 KD cells], showed inverse reactions to toxin-induced membrane damage: ASM KD cells displayed reduced toxin resistance, decreased viability, and defects in membrane repair. In contrast, the down-regulation of NSM-2 led to an increase in viability and enhanced plasmalemmal repair. Yet, in addition to the increased plasmalemmal repair, the enhanced toxin resistance of NSM-2 KD cells also appeared to be dependent on the activation of p38/MAPK, which was constitutively activated, whereas in ASM KD cells, the p38/MAPK activation was constitutively blunted.Schoenauer, R., Larpin, Y., Babiychuk, E. B., Drucker, P., Babiychuk, V. S., Avota, E., Schneider-Schaulies, S., Schumacher, F., Kleuser, B., Koffel, R., Draeger, A. Down-regulation of acid sphingomyelinase and neutral sphingomyelinase-2 inversely determines the cellular resistance to plasmalemmal injury by pore-forming toxins.