Birefringence determination of magnetic moments of magnetotactic bacteria

A birefringence technique is used to determine the average magnetic moments <μ> of magnetotactic bacteria in culture. Differences in <μ> are noted between live and dead bacteria, as well as between normal density and high density samples of live bacteria.     

What controls variation in carbon use efficiency among Amazonian tropical forests?

Why do some forests produce biomass more efficiently than others? Variations in Carbon Use Efficiency (CUE: total Net Primary Production (NPP)/ Gross Primary Production (GPP)) may be due to changes in wood residence time (Biomass/NPP_wood), temperature, or soil nutrient status. We tested these hypotheses in 14, one ha plots across Amazonian and Andean forests where we measured most key components of net primary production (NPP: wood, fine roots, and leaves) and autotrophic respiration (R_a; wood, rhizosphere, and leaf respiration). We found that lower fertility sites were less efficient at producing biomass and had higher rhizosphere respiration, indicating increased carbon allocation to belowground components. We then compared wood respiration to wood growth and rhizosphere respiration to fine root growth and found that forests with residence times <40 yrs had significantly lower maintenance respiration for both wood and fine roots than forests with residence times >40 yrs. A comparison of rhizosphere respiration to fine root growth showed that rhizosphere growth respiration was significantly greater at low fertility sites. Overall, we found that Amazonian forests produce biomass less efficiently in stands with residence times >40 yrs and in stands with lower fertility, but changes to long‐term mean annual temperatures do not impact CUE.     

TWEAK affects keratinocyte G2/M growth arrest and induces apoptosis through the translocation of the AIF protein to the nucleus

The soluble TNF-like weak inducer of apoptosis (TWEAK, TNFSF12) binds to the fibroblast growth factor-inducible 14 receptor (FN14, TNFRSF12A) on the cell membrane and induces multiple biological responses, such as proliferation, migration, differentiation, angiogenesis and apoptosis. Previous reports show that TWEAK, which does not contain a death domain in its cytoplasmic tail, induces the apoptosis of tumor cell lines through the induction of TNFα secretion. TWEAK induces apoptosis in human keratinocytes. Our experiments clearly demonstrate that TWEAK does not induce the secretion of TNFα or TRAIL proteins. The use of specific inhibitors and the absence of procaspase-3 cleavage suggest that the apoptosis of keratinocytes follows a caspase- and cathepsin B-independent pathway. Further investigation showed that TWEAK induces a decrease in the mitochondrial membrane potential of keratinocytes. Confocal microscopy showed that TWEAK induces the cleavage and the translocation of apoptosis inducing factor (AIF) from the mitochondria to the nucleus, thus initiating caspase-independent apoptosis. Moreover, TWEAK induces FOXO3 and GADD45 expression, cdc2 phosphorylation and cdc2 and cyclinB1 degradation, resulting in the arrest of cell growth at the G2/M phase. Finally, we report that TWEAK and FN14 are normally expressed in the basal layer of the physiological epidermis and are greatly enhanced in benign (psoriasis) and malignant (squamous cell carcinoma) skin pathologies that are characterized by an inflammatory component. TWEAK might play an essential role in skin homeostasis and pathology.     

Chitinolytic activity of endophytic Streptomyces and potential for biocontrol

Aims: Biological sources for the control of plant pathogenic fungi remain an important objective for sustainable agricultural practices. Actinomycetes are used extensively in the pharmaceutical industry and agriculture owing to their great diversity in enzyme production. In the present study, therefore, we evaluated chitinase production by endophytic actinomycetes and the potential of this for control of phytopathogenic fungi. Methods and Results: Endophytic Streptomyces were grown on minimum medium supplemented with chitin, and chitinase production was quantified. The strains were screened for any activity towards phytopathogenic fungi and oomycetes by a dual‐culture in vitro assay. The correlation between chitinase production and pathogen inhibition was calculated and further confirmed on Colletotrichum sublineolum cell walls by scanning electron microscopy. Conclusions: This paper reports a genetic correlation between chitinase production and the biocontrol potential of endophytic actinomycetes in an antagonistic interaction with different phytopathogens, suggesting that this control could occur inside the host plant. Significance and Impact of the Study: A genetic correlation between chitinase production and pathogen inhibition was demonstrated. Our results provide an enhanced understanding of endophytic Streptomyces and its potential as a biocontrol agent. The implications and applications of these data for biocontrol are discussed.     

Schistosoma mansoni infection enhances host portal vein contraction: role of potassium channels and p38 MAP kinase

Murine Schistosoma mansoni infection is related to an increased contraction of portal vein in response to 5-hydroxytryptamine (5-HT). The present study addressed a putative alteration of ion channels and enzymes involved in vascular contraction. In control group, either inhibition of K+ channels sensitive to ATP (K(ATP)) or Ca2+ (BK(Ca)) increased 5-HT-induced contraction, but the same did not occur in infected mice. On the other hand, inhibition of p38 MAP kinase markedly decreased the vascular contraction to 5-HT in the infected mice with minor effects in the control group. Accordingly, we observed a higher density of phospho-p38 MAP kinase, that refers to the fully active state of the enzyme, in portal veins from infected mice as compared to control animals. These results suggest that the reduced function of K(ATP) and BK(Ca) channels along with an increased contribution of p38 MAP kinase contribute to the increased contraction of portal veins to 5-HT observed in murine schistosomiasis.     

Global patterns in anuran–prey networks: structure mediated by latitude

Life on Earth is supported by an infinite number of interactions among organisms. Species interactions in these networks are influenced by latitude, evolutionary history and species traits. We performed a global‐scale literature analysis to build up a database of interactions between anuran communities and their preys, from a wide range of geographical areas, using a network approach. For this purpose, we compiled a total of 55 weighted anuran–prey interaction networks, 39 located in the tropics and 16 in temperate areas. We tested the influence of latitude, as well as anuran taxonomic, functional and phylogenetic richness on network metrics. We found that anuran–prey networks are not nested, exhibit low complementary specialization and modularity and high connectance when compared to other types of networks. The main effects on network metrics were related to latitude, followed by anuran taxonomic, functional and phylogenetic richness, a pattern similar to the emerging in mutualistic networks. Our study is the first integrated analysis of the structural patterns in anuran–prey antagonistic interaction networks in different parts of the world. We suggest that different processes, mediated mainly by latitude, are modeling the architecture of anuran–prey networks across the globe.     

Double-strand breaks and tumorigenesis.

The establishment of connections between biochemical defects and clinical disease is a major goal of modern molecular genetics. In this review, we examine the current literature that relates defects in the two major DNA double-strand-break repair pathways--homologous recombination and nonhomologous end-joining--with the development of human tumors. Although definitive proof has yet to be obtained, the current literature is highly suggestive of such a link.     

The Role of Chromosome Missegregation in Cancer Development: A Theoretical Approach Using Agent-Based Modelling

Many cancers are aneuploid. However, the precise role that chromosomal instability plays in the development of cancer and in the response of tumours to treatment is still hotly debated. Here, to explore this question from a theoretical standpoint we have developed an agent-based model of tissue homeostasis in which to test the likely effects of whole chromosome mis-segregation during cancer development. In stochastic simulations, chromosome mis-segregation events at cell division lead to the generation of a diverse population of aneuploid clones that over time exhibit hyperplastic growth. Significantly, the course of cancer evolution depends on genetic linkage, as the structure of chromosomes lost or gained through mis-segregation events and the level of genetic instability function in tandem to determine the trajectory of cancer evolution. As a result, simulated cancers differ in their level of genetic stability and in their growth rates. We used this system to investigate the consequences of these differences in tumour heterogeneity for anti-cancer therapies based on surgery and anti-mitotic drugs that selectively target proliferating cells. As expected, simulated treatments induce a transient delay in tumour growth, and reveal a significant difference in the efficacy of different therapy regimes in treating genetically stable and unstable tumours. These data support clinical observations in which a poor prognosis is correlated with a high level of chromosome mis-segregation. However, stochastic simulations run in parallel also exhibit a wide range of behaviours, and the response of individual simulations (equivalent to single tumours) to anti-cancer therapy prove extremely variable. The model therefore highlights the difficulties of predicting the outcome of a given anti-cancer treatment, even in cases in which it is possible to determine the genotype of the entire set of cells within the developing tumour.