Picus leuconotus in B?hmen erlegt

Ohne Zusammenfassung     

Darwin teleologist? Design in the Orchids

Focusing on the Orchids, this article aims at disentangling the concepts of teleology, design and natural theology. It refers to several contemporary critics of Darwin (Kölliker, Argyll, Royer, Candolle, Delpino) to challenge Huxley's interpretation that Darwin's system was “a deathblow” to teleology. The Orchids seem rather to be a “flank-movement” (Gray): it departs from the Romantic theories of transmutation and the “imaginary examples” of the Origin; it focuses on empirical data and on teleological structures. Although Darwin refers to natural selection, his readers mock him for his fascination for delicate morphological contrivances and co-adaptations – a sign that he was inescapably lured to finality. Some even suggested that his system was a “theodicy”. In the history of Darwinism, the Orchids reveal “another” quite unexpected and heterodox Darwin: freed from the hypothetical fancies of the Origin, and even suggesting a new kind of physico-theology.     

Acetate accumulation through alternative metabolic pathways in ackA?pta?poxB? triple mutant in E. coli B (BL21)

Individual deletions of acs and aceA genes in E. coli B (BL21) showed little difference in the metabolite accumulation patterns but deletion of the ackA gene alone or together with pta showed acetic acid gradually accumulated to 3.1 and 1.7 g/l, respectively, with a minimal extended lag in bacterial growth and a higher pyruvate formation. Single poxB deletion in E. coli B (BL21) or additional poxB deletion in the ackA-pta mutants did not change the acetate accumulation pattern. When the acetate production genes (ackA-pta-poxB) were deleted in E. coli B (BL21) acetate still accumulated. This may be an indication that perhaps acetate is not only a by-product of carbon metabolism; it is possible that acetate plays also a role in other cellular metabolite pathways. It is likely that there are alternative acetate production pathways.     

Red-mediated recombination of phage lambda in a recA? recB?host

Summary The lambda Red recombination system works poorly among unreplicated gam ⁺ lambda chromosomes in recA ^- cells compared to recA ⁺ cells. Recombination is not enhanced in recA ^- recB^-cells. Thus, the inability of Red to promote recombination in recA ^- replication-blocked cross is not due to the hypothetical destruction of recombination intermediates by the recB nuclease. This conclusion strengthens previous proposals that the products of the red genes can operate upon recombinational intermediates which require recA activity for their formation.     

Nampt/PBEF/Visfatin: a new player in beta cell physiology and in metabolic diseases?

NAD plays an essential role in a number of biological processes. A study in this issue of Cell Metabolism (Revollo et al., 2007b) demonstrates that nicotinamide phosphoribosyltransferase (Nampt), also known as PBEF or visfatin, is a secreted enzyme and a source of systemic NAD. The authors show that Nampt-mediated NAD synthesis is necessary for beta cell function, providing fresh insights into the pathophysiology of metabolic diseases.     

Ethanol-hypersensitive and ethanol-dependent cdc? mutants in Schizosaccharomyces pombe

Ethanol-hypersensitive strains (ets mutants), unable to grow on media containing 6% ethanol, were isolated from a sample of mutagenized Schizosaccharomyces pombe wild-type cells. Genetic analysis of these ets strains demonstrated that the ets phenotype is associated with mutations in a large set of genes, including cell division cycle (cdc) genes, largely non-overlapping with the set represented by the temperature conditional method; accordingly, we isolated some ets non-ts cdc ^– mutants, which may identify novel essential genes required for regulation of the S. pombe cell cycle. Conversely, seven well characterized ts cdc ^– mutants were tested for their ethanol sensitivity; among them, cdc1–7 and cdc13–117 exhibited a tight ets phenotype. Ethanol sensitivity was also tested in strains bearing different alleles of the cdc2 gene, and we found that some of them were ets, but others were non-ets; thus, ethanol hypersensitivity is an allele-specific phenotype. Based on the single base changes found in each particular allele of the cdc2 gene, it is shown that a single amino acid substitution in the p34^cdc2 gene product can produce this ets phenotype, and that ethanol hypersensitivity is probably due to the influence of this alcohol on the secondary and/or tertiary structure of the target protein. Ethanol-dependent (etd) mutants were also identified as mutants that can only be propagated on ethanol-containing media. This novel type of conditional phenotype also covers many unrelated genes. One of these etd mutants, etd1-1, was further characterized because of the lethal cdc ^– phenotype of the mutant cells under restrictive conditions (absence of ethanol). The isolation of extragenic suppressors of etd1-1, and the complementation cloning of a DNA fragment encompassing the etd1 ⁺ wild-type gene (or an extragenic multicopy suppressor) demonstrate that current genetic techniques may be applied to mutants isolated by using ethanol as a selective agent.     

β-N-Acetylhexosaminidase: What's in a name…?

β-N-Acetylhexosaminidases (EC 3.2.1.52, belonging to CAZy GH families 3, 20 and 84) have recently gained a lot of attention, not only due to their implication in human physiology and disease, but also due to their great potential in the enzymatic synthesis of carbohydrates and glycomimetics. GH family 20 β-N-acetylhexosaminidases, and GH family 3 and 84 β-N-acetylglucosaminidases from all kinds of organisms have been intensively studied from the point of view of their physiological roles, reaction mechanisms, structure and inhibition. Thanks to their outstanding substrate promiscuity, extracellular β-N-acetylhexosaminidases from filamentous fungi are able to cleave and transfer substrates bearing various functionalities, ranging from carboxylates, sulfates, acylations to azides, and even 4-deoxy glycosides. Thus, they have proved to be versatile biosynthetic tools for the preparation of both natural and modified hexosaminides under mild conditions with good yields.     

Is Giardia a significant pathogen in production animals?

Although Giardia duodenalis is recognised worldwide as the most important parasitic cause of gastro-intestinal disorder in human patients, the relevance of infection in production animals is prone to debate. Since the 1980s, clinical disease has been associated with giardiasis in production animals, both in natural conditions and in experimental studies. However, most Giardia research is focussed on the relevance of production animals as a reservoir for zoonotic transmission. In this study, the current knowledge on clinical relevance of giardiasis in production animals is reviewed, along with the diagnosis, treatment and control of infection. Furthermore, future research objectives are discussed.     

Adaptive value of polymorphism in intracellular self/not-self discrimination?

A microbial pathogen species can adapt to its host species to the extent that members of the host species are uniform. Loss of this uniformity would make it difficult for a pathogen species to transfer, from one member of the host species to another, what it had "learned" through selection of its members with advantageous mutations. The existence of major histocompatibility complex (MHC) polymorphism indicates that non-uniformity within a species is an effective host defence strategy. By virtue of this molecular discontinuity among its members the host species can "present a moving target" to the pathogen. Many proteins other than MHC proteins show polymorphism - a phenomenon which has suggested that mutations in regions of protein molecules which do not affect overt function are neutral. However, in the context of the author's differential aggregation theory of intracellular self/not-self discrimination as previously applied to the problem of the antigenicity of cancer cells, such polymorphism should serve for the recruitment of subsets of self-antigens into the antigenic repertoire of an infected cell. These would act as "intracellular antibodies" by virtue of their weak, but specific, aggregation with pathogen proteins. Peptides from the self-antigens, as well as (or instead of) those from the antigens of the pathogen, would then serve as targets for attack by cytotoxic T cells. Thus, polymorphism of intracellular proteins should be of adaptive value, serving to amplify and individualize the immune response to intracellular pathogens.     

Trichoderma harzianum strain T-22 induces changes in phytohormone levels in cherry rootstocks (Prunus cerasus?×?P. canescens)

The aim of this research was to explain the direct plant growth-promoting activity of Trichoderma harzianum strain T-22 (T22), hypothesizing the involvement of different classes of plant growth regulators. Seven days after the transfer to root-inducing medium, in vitro-cultured shoots of GiSeLa6^? (Prunus cerasus  × P. canescens) were inoculated with T22. Root and shoot growth were significantly affected by T22 (+76 and +61%, respectively). Ten days after inoculation, the levels of indole-3-acetic acid (IAA), trans-zeatin riboside (t-ZR), dihydrozeatin riboside (DHZR), gibberellic acid (GA3) and abscisic acid (ABA) were analyzed by high performance liquid chromatography coupled with mass spectrometry. The results showed that after T22-inoculation, IAA and GA3 significantly increased in both leaves (+49 and +71%, respectively) and roots (+40 and +143%, respectively) whereas t-ZR decreased (−51% in leaves and −37% in roots). Changes in DHZR were observed in T22-inoculated roots (−32%) but not in leaves, whereas the levels of ABA did not differ between the two treatments. The extraction method allowed the simultaneous extraction of phytohormones. There is evidence that the change in phytohormone levels is one of the direct mechanism by which T22 promotes rooting and shoot growth, with notable advantages for rootstock production during nursery processes.     

Polymorphisms in the CD28/CTLA4/ICOS genes: role in malignant melanoma susceptibility and prognosis?

The appearance of vitiligo and spontaneous regression of the primary lesion in melanoma patients illustrate a relationship between tumor immunity and autoimmunity. T lymphocytes play a major role both in tumor immunity and autoimmunity. CD28, Cytotoxic T lymphocyte antigen 4 (CTLA4) and inducible costimulator (ICOS) molecules are important secondary signal molecules in the T lymphocyte activation. Single nucleotide polymorphisms (SNPs) in the CD28/CTLA4/ICOS gene region were reported to be associated with several autoimmune diseases including, type-1 diabetes, SLE, autoimmune thyroid diseases and celiac disease. In this study, we investigated the association of SNPs in the CD28, CTLA4 and ICOS genes with the risk of melanoma. We also assessed the prognostic effect of the different polymorphisms in melanoma patients. Twenty-four tagging SNPs across the three genes and four additional SNPs were genotyped in a cohort of 763 German melanoma patients and 734 healthy German controls. Influence on prognosis was determined in 587 melanoma cases belonging to stage I or II of the disease. In general, no differences in genotype or allele frequencies were detected between melanoma patients and controls. However, the variant alleles for two polymorphisms in the CD28 gene were differentially distributed in cases and controls. Similarly no association of any polymorphism with prognosis, except for the rs3181098 polymorphism in the CD28 gene, was observed. In addition, individuals with AA genotype for rs11571323 polymorphism in the ICOS gene showed reduced overall survival. However, keeping in view the correction for multiple hypothesis testing our results suggest that the polymorphisms in the CD28, CTLA4 and ICOS genes at least do not modulate risk of melanoma and nor do those influence the disease prognosis in the investigated population.     

Neuroscience in recession?

As the global financial downturn continues, its impact on neuroscientists - both on an individual level and at the level of their research institute - becomes increasingly apparent. How is the economic crisis affecting neuroscience funding, career prospects, international collaborations and scientists' morale in different parts of the world? Nature Reviews Neuroscience gauged the opinions of a number of leading neuroscientists: the President of the Society for Neuroscience, the President Elect of the British Neuroscience Association, the former President of the Japan Neuroscience Society, the President of the Federation of European Neuroscience Societies and the Director of the US National Institute of Mental Health. Their responses provide interesting and important insights into the regional impact of the global financial downturn, with some causes for optimism for the future of neuroscience research.