The impact of vegetation characteristics and prey availability on breeding habitat use and diet of Little Owls Athene noctua in Central European farmland

Capsule Foraging habitats are determined by vegetation characteristics rather than the availability of insect prey.

Aims To determine the diet composition of Little Owls in relation to the availability of insects at foraging sites, and to elucidate the main factors determining the owls’ habitat choice.

Methods The feeding ecology of Little Owls was studied during the 2002 breeding season in the agricultural landscape of western Bohemia (Czech Republic), where its population is in decline. Diet composition was determined by pellet analysis. Insect availability was studied using pitfall traps in the two most important Little Owl foraging habitats. For both habitats, we assessed the main vegetative characteristics (average and maximum vegetation height, vegetation density).

Results Based on number, insects were the most dominant prey, followed by small mammals; based on weight, insects comprised only a minor part of the diet. Among insect prey, Carabidae beetles were the most abundant. The proportion of insect numbers was strongly positively correlated with advancing day of the season and negatively correlated with the proportion of vertebrates. Although the highest densities of Carabidae were found in cornfields Little Owls significantly preferred grassland habitats, probably because of the lower vegetation cover.

Conclusions The availability of short sward vegetation in grassland habitats during the breeding season may play a key role in the conservation of Little Owls in central European farmland.     

Assessment of variation of nest survival for grassland birds due to method of nest discovery

Capsule Interpretation of nest survival estimates may be improved by incorporating the search method used to locate nests as a covariate.

Aims To compare annual survival estimates for Dickcissel Spiza americana nests and determine if incorporating search method (structured, opportunistic, or behavioural searches) improved model fit.

Methods Dickcissel nests were located using structured, opportunistic, or behavioural searches over three years (2011–2013) in Mississippi, USA. Models were used to estimate daily survival rates (DSRs) and to analyse factors influencing nest survival.

Results DSRs for Dickcissels were best explained by quadratic date, nest age, age found, and year, but incorporating search method improved model fit. Daily survival was 1.51 times greater for nests located using opportunistic search methods relative to structured searches, but was not significantly different between structured and behavioural searches.

Conclusions Survival estimates varied by search method, specifically between structured searches and opportunistically located nests. This might have arisen because heterogeneity in nest placement or parental behaviour may influence the sample of nests located with a given search method. Researchers may be able to account for this potential source of bias by including search method as a model covariate when using standard survey designs or modelling approaches.     

Dramatic changes in the return date of Guillemots Uria aalge to colonies in Shetland, 1962–2005

Capsule Changes in return date coincided with marked changes in population size that probably resulted in fluctuating competition for nest-sites.

Aims To document the changes in return dates over a 44-year period and to identify the factors associated with these changes.

Methods We compared changes in return date at Shetland colonies with those for the Isle of May, southeast Scotland, and with the available information on population size, the abundance of some fish species eaten by Common Guillemots and large-scale changes in the oceanography and climate of the eastern Atlantic as reflected by the winter index of the North Atlantic Oscillation (NAO).

Results Common Guillemots normally return to colonies in Shetland in late winter. However, during the 1960s return dates became gradually earlier with birds present from early October. Autumn return remained the norm for about ten years after which return dates gradually reverted back to late winter. In contrast, Common Guillemots on the Isle of May, 400 km south of Shetland, showed no marked shift, returning in October each year. There was a strong negative correlation between date of return of Shetland birds and population size, whereas on the Isle of May birds came back earlier when there was a large positive winter NAO index. There was no convincing evidence that changes in wintering areas or fish abundance influenced when birds returned to the colonies, although the fish data may not have been collected on the correct spatial scale.

Conclusion Competition for high quality nest-sites is the most likely reason for Common Guillemots returning to the colonies during the autumn and winter.     

Osmotic Challenge Drives Rapid and Reversible Chromatin Condensation in Chondrocytes

Changes in extracellular osmolality have been shown to alter gene expression patterns and metabolic activity of various cell types, including chondrocytes. However, mechanisms by which physiological or pathological changes in osmolality impact chondrocyte function remain unclear. Here we use quantitative image analysis, electron microscopy, and a DNase I assay to show that hyperosmotic conditions (>400 mOsm/kg) induce chromatin condensation, while hypoosmotic conditions (100 mOsm/kg) cause decondensation. Large density changes (p < 0.001) occur over a very narrow range of physiological osmolalities, which suggests that chondrocytes likely experience chromatin condensation and decondensation during a daily loading cycle. The effect of changes in osmolality on nuclear morphology (p < 0.01) and chromatin condensation (p < 0.001) also differed between chondrocytes in monolayer culture and three-dimensional agarose, suggesting a role for cell adhesion. The relationship between condensation and osmolality was accurately modeled by a polymer gel model which, along with the rapid nature of the chromatin condensation (<20 s), reveals the basic physicochemical nature of the process. Alterations in chromatin structure are expected to influence gene expression and thereby regulate chondrocyte activity in response to osmotic changes.     

The Small Heat Shock Protein Hsp27 Affects Assembly Dynamics and?Structure of Keratin Intermediate Filament Networks

The mechanical properties of living cells are essential for many processes. They are defined by the cytoskeleton, a composite network of protein fibers. Thus, the precise control of its architecture is of paramount importance. Our knowledge about the molecular and physical mechanisms defining the network structure remains scarce, especially for the intermediate filament cytoskeleton. Here, we investigate the effect of small heat shock proteins on the keratin 8/18 intermediate filament cytoskeleton using a well-controlled model system of reconstituted keratin networks. We demonstrate that Hsp27 severely alters the structure of such networks by changing their assembly dynamics. Furthermore, the C-terminal tail domain of keratin 8 is shown to be essential for this effect. Combining results from fluorescence and electron microscopy with data from analytical ultracentrifugation reveals the crucial role of kinetic trapping in keratin network formation.     

Identification of a new membrane-permeable inhibitor against inositol-1,4,5-trisphosphate-3-kinase A

Ectopic expression of the neuron-specific inositol-1,4,5-trisphosphate-3-kinase A (ITPKA) in lung cancer cells increases their metastatic potential because the protein exhibits two actin regulating activities; it bundles actin filaments and regulates inositol-1,4,5-trisphosphate (InsP₃)-mediated calcium signals by phosphorylating InsP₃. Thus, in order to inhibit the metastasis-promoting activity of ITPKA, both its actin bundling and its InsP₃kinase activity has to be blocked. In this study, we performed a high throughput screen in order to identify specific and membrane-permeable substances against the InsP₃kinase activity. Among 341,44 small molecules, 237 compounds (0.7%) were identified as potential InsP₃kinase inhibitors. After determination of IC₅₀-values, the three compounds with highest specificity and highest hydrophobicity (EPPC-3, BAMB-4, MEPTT-3) were further characterized. Only BAMB-4 was nearly completely taken up by H1299 cells and remained stable after cellular uptake, thus exhibiting a robust stability and a high membrane permeability. Determination of the inhibitor type revealed that BAMB-4 belongs to the group of mixed type inhibitors. Taken together, for the first time we identified a highly membrane-permeable inhibitor against the InsP₃kinase activity of ITPKA providing the possibility to partly inhibit the metastasis-promoting effect of ITPKA in lung tumor cells.     

Constitutive Activation of the Calcium Sensor STIM1 Causes Tubular-Aggregate Myopathy

Tubular aggregates are regular arrays of membrane tubules accumulating in muscle with age. They are found as secondary features in several muscle disorders, including alcohol- and drug-induced myopathies, exercise-induced cramps, and inherited myasthenia, but also exist as a pure genetic form characterized by slowly progressive muscle weakness. We identified dominant STIM1 mutations as a genetic cause of tubular-aggregate myopathy (TAM). Stromal interaction molecule 1 (STIM1) is the main Ca²⁺ sensor in the endoplasmic reticulum, and all mutations were found in the highly conserved intraluminal Ca²⁺-binding EF hands. Ca²⁺ stores are refilled through a process called store-operated Ca²⁺ entry (SOCE). Upon Ca²⁺-store depletion, wild-type STIM1 oligomerizes and thereby triggers extracellular Ca²⁺ entry. In contrast, the missense mutations found in our four TAM-affected families induced constitutive STIM1 clustering, indicating that Ca²⁺ sensing was impaired. By monitoring the calcium response of TAM myoblasts to SOCE, we found a significantly higher basal Ca²⁺ level in TAM cells and a dysregulation of intracellular Ca²⁺ homeostasis. Because recessive STIM1 loss-of-function mutations were associated with immunodeficiency, we conclude that the tissue-specific impact of STIM1 loss or constitutive activation is different and that a tight regulation of STIM1-dependent SOCE is fundamental for normal skeletal-muscle structure and function.     

Inhibition of GATE-16 attenuates ATRA-induced neutrophil differentiation of APL cells and interferes with autophagosome formation

Autophagy is an intracellular bulk degradation process involved in cell survival upon stress induction, but also with a newly identified function in myeloid differentiation. The autophagy-related (ATG)8 protein family, including the GABARAP and LC3 subfamilies, is crucial for autophagosome biogenesis. In order to evaluate the significance of the GABARAPs in the pathogenesis of acute myeloid leukemia (AML), we compared their expression in primary AML patient samples, CD34⁺ progenitor cells and in granulocytes from healthy donors. GABARAPL1 and GABARAPL2/GATE-16, but not GABARAP, were significantly downregulated in particular AML subtypes compared to normal granulocytes. Moreover, the expression of GABARAPL1 and GATE-16 was significantly induced during ATRA-induced neutrophil differentiation of acute promyelocytic leukemia cells (APL). Lastly, knocking down GABARAPL2/GATE-16 in APL cells attenuatedneutrophil differentiation and decreased autophagic flux. In conclusion, low GABARAPL2/GATE-16 expression is associated with an immature myeloid leukemic phenotype and these proteins are necessary for neutrophil differentiation of APL cells.     

The first case of fatal pneumonia caused by Panton–Valentine leukocidin-producing Staphylococcus aureus in an infant in the Czech Republic

Panton–Valentine leukocidin-producing strains of Staphylococcus aureus can cause severe skin and soft tissue infections and necrotizing pneumonia with a high mortality rate. This is a report on the first case of fatal pneumonia with mediastinitis in an infant in the Czech Republic. The causative agent was a methicillin-susceptible S. aureus strain with pronounced production of the PVL toxin and hyperproduction of enterotoxin A.