Drosophila caspase transduces Shaggy/GSK-3beta kinase activity in neural precursor development

Caspases are well known for their role in the execution of apoptotic programs, in which they cleave specific target proteins, leading to the elimination of cells, and for their role in cytokine maturation. In this study, we identified a novel substrate, which, through cleavage by caspases, can regulate Drosophila neural precursor development. Shaggy (Sgg)46 protein, an isoform encoded by the sgg gene and essential for the negative regulation of Wingless signaling, is cleaved by the Dark-dependent caspase. This cleavage converts it to an active kinase, which contributes to the formation of neural precursor (sensory organ precursor (SOP)) cells. Our evidence suggests that caspase regulation of the wingless pathway is not associated with apoptotic cell death. These results imply a novel role for caspases in modulating cell signaling pathways through substrate cleavage in neural precursor development.     

Correlation between structure and temperature in prokaryotic metabolic networks

Background  

In recent years, an extensive characterization of network structures has been made in an effort to elucidate design principles of metabolic networks, providing valuable insights into the functional organization and the evolutionary history of organisms. However, previous analyses have not discussed the effects of environmental factors (i.e., exogenous forces) in shaping network structures. In this work, we investigate the effect of temperature, which is one of the environmental factors that may have contributed to shaping structures of metabolic networks.     

SHP-1 Regulation of Mast Cell Function in Allergic Inflammation and Anaphylaxis

Allergic inflammation and severe allergic reactions (anaphylaxis) are important in allergen induced diseases. Bacterial products such as lipopolysaccharide (LPS) are ubiquitous and can facilitate allergen induced Th2 immune responses. Phosphatase SHP-1 is critical in regulating immunological homeostasis and in allergen induced Th2 immune responses in the lung. However, the mechanisms underlying the initiation of allergic inflammation and allergen induced anaphylaxis are still not completely elucidated and it is unclear whether SHP-1 plays any role in LPS-induced airway inflammation and in allergen-induced anaphylaxis. In this study we tested the hypothesis that phosphatase SHP-1 plays an important role in allergic inflammation and anaphylaxis and determined whether its effects are through regulation of mast cell functions. SHP-1 deficient (mev/+ and mev/mev) and mast cell deficient (Kit^W-sh) mice were examined in their responses to LPS airway stimulation and to ovalbumin (OVA) allergen induced systemic anaphylaxis. Compared to wild type mice, mev/+ mice had significantly enhanced LPS induced airway inflammation and OVA induced anaphylactic responses, including hypothermia and clinical symptoms. These changes were mast cell dependent as Kit^W-sh mice had reduced responses whereas adoptive transfer of mast cells restored the responses. However, T and B cells were not involved and macrophages did not play a significant role in LPS induced airway inflammation. Interestingly, basophil differentiation from SHP-1 deficient bone marrow cells was significantly reduced. These findings provided evidence that through regulation of mast cell functions SHP-1 plays a critical role as a negative regulator in allergic inflammation and in allergen induced anaphylaxis. In addition, SHP-1 seems to be required for normal basophil development.     

Dynamic reorganization of microfilaments and microtubules is necessary for the expression of non-host resistance in barley coleoptile cells

To show the involvement of microfilaments and microtubules in non-host resistance of barley, partially dissected coleoptiles which had been inoculated with a non-pathogen, Erysiphe pisi, were treated with several actin and tubulin inhibitors. If the coleoptiles were not treated with any of the inhibitors, the non-pathogen always failed to penetrate the coleoptile cells. However, when coleoptiles were treated with actin or tubulin polymerization or depolymerization inhibitors, the non-pathogen was able to penetrate successfully and to form haustoria in coleoptile cells of a non-host plant, barley. Actin polymerization inhibitors, cytochalasins, were more effective in causing an increase in penetration efficiency of E. pisi than tubulin inhibitors. The effects of cytochalasins depended on the kind of cytochalasin; the strength of the actin depolymerizing activity correlated significantly with the efficiency of increasing the penetration of the non-pathogen. When both actin and tubulin inhibitors were added simultaneously, the polarization of defense-related responses, such as massive cytoplasmic aggregation, deposition of papillae and accumulation of autofluorescent compounds, at fungal penetration sites was suppressed. Actin inhibitors did not affect arrangement and stability of microtubules and vice versa, and a double treatment of coleoptile cells with both microfilament and microtubule inhibitors showed an additive effect in increasing the penetration efficiency of E. pisi. Furthermore, cytochalasin A treatment allowed other non-pathogens, Colletotrichum lagenarium and Alternaria alternata, to penetrate successfully into the non-host barley cells. These results strongly suggest that microfilaments and microtubules might play important roles in the expression of non-host resistance of barley.     

Cyclic AMP phosphodiesterase in human lymphocytes and lymphoblasts.

Cyclic nucleotide phosphodiesterase activities were examined in lymphocytes from 12 transformed human B cell lines, two T cell lines, six patients with lymphocytic leukemia, and 10 normal donors. A consistent difference bwtween cells from the normal and leukemic state was observed. The cyclic AMP phosphodiesterase activity from normal lymphocytes is inhibited greater than 80% by muM cyclic GMP while this concentration of nucleotide has little or no effect on the enzyme from transformed lymphocytic cell lines or from lymphocytic cells of leukemia patients. The reported lack of cyclic GMP phosphodiesterase in human lymphocytes from several sources is confirmed. The apparent absence of a cyclic GMP degradation mechanism and of cyclic GMP control of cyclic AMP hydrolysis may be related to defective lymphocyte growth control.     

Physical map of the BK virus genome.

Two new human papovavirus isolates (JMV and MMV) from the urines of patients with Wiskott-Aldrich syndrome were morphologically and serologically identical to BK virus (BKV). The genomes of these two new isolates were found to be indistinguishable from prototype BKV DNA in a variety of nucleic acid hybridization experiments. Like BKV DNA, JMV and MMV DNAs share approximately 20% of their polynucleotide sequences with simian virus 40 DNA. The genome of JMV was indistinguishable from that of BKV by restriction endonuclease analysis; MMV DNA contained three instead of four R-Hind cleavage sites and one rather than no R-HpaII cleavage sites. Physical maps of the BKV and MMV genomes were constructed using restriction endonucleases, and these maps were oriented to the map of simian virus 40 DNA.     

The structure of syringomycins A1, E and G

By a combination of 1D and 2D 1H- and 13C-NMR, FAB-MS, and chemical and enzymatic reactions carried out at the milligram level, it has been demonstrated that syringomycin E, the major phytotoxic antibiotic produced by Pseudomonas syringae pv. syringae, is a new lipodepsipeptide. Its amino acid sequence is Ser-Ser-Dab-Dab-Arg-Phe-Dhb-4(Cl)Thr-3(OH)Asp with the beta-carboxy group of the C-terminal residue closing a macrocyclic ring on the OH group of the N-terminal Ser, which in turn is N-acylated by 3-hydroxydodecanoic acid. Syringomycins A1 and G, two other metabolites of the same bacterium, differ from syringomycin E only in their fatty acid moieties corresponding, respectively, to 3-hydroxydecanoic and 3-hydroxytetradecanoic acid.     

Gap junctions from the lens: Purification and characterization by chemical crosslinking reagent

Quantitation of gap junction preparations from chick lens by transmission electron microscopy has indicated that 95.0% of the membrane bilayer material is in the form trilayer structures. The preparations were comprised of a major polypeptide component of 26K, as well as minor components of 49K, 46K and 22K–15K. Treatment with oxidizing agent resulted in the production of apparent homo-oligomeric complexes involving the 26K and 46K components. These results demonstrate that the 26K polypeptide is the major component of highly purified preparations of lens gap junctions. Furthermore, they demonstrate that this 26K component plus an additional 46K component are both involved in extensive nearest-neighbor interactions in the intact junctional complex.     

Pathogenicity and taxonomy of Tenuignomonia styracis gen. et sp. nov., a new monotypic genus of Gnomoniaceae on Styrax obassia in Japan

Since 2010, an unknown fungus in the Gnomoniaceae has been found on overwintered leaves and petioles of Styrax obassia (Styracaceae) in Japan. This fungus is characterized by dark brown immersed or partially erumpent ascomata with long necks and fusiform to obovoid asci each with an acute or long tapering stipe. Each ascus bears eight fusiform to filiform ascospores. Our morphological observation and phylogenetic analyses based on the markers LSU, rpb2, and tef-1α indicated that this is a new monotypic genus in the Gnomoniaceae (Diaporthales), and Tenuignomonia styracis gen. et sp. nov. was descried herein. Members of the Gnomoniaceae are commonly isolated as endophytes, saprobes, and plant pathogens from a broad diversity of herbaceous, shade tree, and agriculturally significant plants. We thus carried out a pathogenicity test to determine if T. styracis is the causative agent of leaf blotch on S. obassia. One week after inoculation, this fungus produced small necrotic spots on the leaves and petioles, and all leaves having necrotic spots were abscised in a short time. We thus confirmed that this fungus has weak pathogenicity on S. obassia. This new species may promote early defoliation of S. obassia during the fall.