Using ecological networks to answer questions in global biogeography and ecology

Ecological networks have classically been studied at site and landscape scales, yet recent efforts have been made to collate these data into global repositories. This offers an opportunity to integrate and upscale knowledge about ecological interactions from local to global scales to gain enhanced insights from the mechanistic information provided by these data. By drawing on existing research investigating patterns in ecological interactions at continental to global scales, we show how data on ecological networks, collected at appropriate scales, can be used to generate an improved understanding of many aspects of ecology and biogeography—for example, species distribution modelling, restoration ecology and conservation. We argue that by understanding the patterns in the structure and function of ecological networks across scales, it is possible to enhance our understanding of the natural world.     

Total chemical synthesis and NMR characterization of the glycopeptide tx5a, a heavily post-translationally modified conotoxin, reveals that the glycan structure is alpha-D-Gal-(1-->3)-alpha-D-GalNAc.

The 13-amino acid glycopeptide tx5a (Gla-Cys-Cys-Gla-Asp-Gly-Trp*-Cys-Cys-Thr*-Ala-Ala-Hyp-OH, where Trp* = 6-bromotryptophan and Thr* = Gal-GalNAc-threonine), isolated from Conus textile, causes hyperactivity and spasticity when injected intracerebral ventricularly into mice. It contains nine post-translationally modified residues: four cysteine residues, two gamma-carboxyglutamic acid residues, and one residue each of 6-bromotryptophan, 4-trans-hydroxyproline and glycosylated threonine. The chemical nature of each of these has been determined with the exception of the glycan linkage pattern on threonine and the stereochemistry of the 6-bromotryptophan residue. Previous investigations have demonstrated that tx5a contains a disaccharide composed of N-acetylgalactosamine (GalNAc) and galactose (Gal), but the interresidue linkage was not characterized. We hypothesized that tx5a contained the T-antigen, beta-D-Gal-(1-->3)-alpha-D-GalNAc, one of the most common O-linked glycan structures, identified previously in another Conus glycopeptide, contalukin-G. We therefore utilized the peracetylated form of this glycan attached to Fmoc-threonine in an attempted synthesis. While the result-ing synthetic peptide (Gla-Cys-Cys-Gla-Asp-Gly-Trp*-Cys-Cys-Thr*-Ala-Ala-Hyp-OH, where Trp* =6-bromotryptophan and Thr* = beta-D-Gal-(1-->3)-alpha-D-GalNAc-threonine) and the native peptide had almost identical mass spectra, a comparison of their RP-HPLC chromatograms suggested that the two forms were not identical. Two-dimensional 1H homonuclear and 13C-1H heteronuclear NMR spectroscopy of native tx5a isolated from Conus textile was then used to determine that the glycan present on tx5a indeed is not the aforementioned T-antigen, but rather alpha-D-Gal-(1-->3)-alpha-D-GalNAc.     

Historical biogeography and morphological differentiation ofStreptocephalus torvicornis (Waga) since the Würm III-glaciation

We argue that the Würm III glaciation eradicated possible European populations ofS. torvicornis, and that today, a reconquest of Europe takes place on two fronts.A western wave has reached the Pyrenees, an eastern one now occupies most of eastern and northern Europe. The western route probably started in the Maghreb, the eastern one in the Levant and the Ponto-Caspian. Animals in the west had to move north by crossing, at right angles, a series of east-west oriented river valleys and progressed slowly; animals in the east could move up river valleys extending north-east, and moved quickly. Italy was not occupied, becauseS.torvicornis is a warm stenotherm, and by the time the climate had warmed sufficiently for it to reach the southern shore of the mediterranean (ca 6000 BP), the gap with Italy was probably too large for a crossing. Cold-loving species (of the generaBranchipus, Chirocephalus) conversely, and could freely flow across the Central Mediterranean at low sea-levels (ca 12000 BP), and now occur in Italy (and the rest of Europe) as well as in Northern Africa.A prediction of our hypothesis is that the pioneer populations in Spain and Central Europe should have been isolated longest. Thisis tested and confirmed by their comparative morphology, and two subspecies,S. t. torvicornis andS. t. bucheti are reinstated.A gap across the Nile Valley where onlyS. rubricaudatus seems to occur, deserves further study.     

Somatic expansion of the (CAG) n repeat in Huntington disease brains

The mutation causing Huntington disease (HD) has been identified as an expansion of a polymorphic (CAG) _n repeat in the 5 part of the huntingtin gene. The specific neuropathology of HD, viz. selective neuronal loss in the caudate nucleus and putamen, cannot be explained by the widespread expression of the gene. Since somatic expansion is observed in affected tissue in myotonic dystrophy, we have studied the length of the (CAG) _n repeat in various regions of the brain. Although we have not found clear differences when comparing severely and mildly affected regions, we have observed a minor increase in repeat length upon comparison of affected brain samples with cerebellum or peripheral blood. Hence, although further somatic amplification seems to occur in affected areas of the brain, the differences between affected and unaffected regions are too small to make this mechanism an obvious candidate for the cause of differential neuronal degeneration in HD.     

Immunological studies on lysosomal sphingomyelinase: Identification of a 28 000-Da component deficient in urine from patients with Niemann-Pick disease types A and B

The immunoblotting technique was used to identify sphingomyeJinase protein in samples of tissue and urine after subjection to poIyacrylamide-gel etectrophoresis in the presence of sodium dodecyl sulphate. In a sphingomyelinase preparation purified from control urine a prominent band was seen with an M_r of 28 000 Da. Glycoprotein fractions from urine and placenta, a membrane extract from spleen, and a partially purified sphingomyelinase preparation from placenta contained the 28 000-Da band plus additional, higher-M_r bands. The 28 000-Da band was detectable in urine from a patient with Niemann-Pick disease type C, but not in urine from patients with Niemann-Pick disease types A and B. It is concluded t h a t sphingomyeJinase is composed of at least one polypeptide with an M_r of 28 000 Da and that this polypeptide is deficient in the urine of patients with Niemann-Pick disease types A and B.     

Effects of bunaftine on morphology,microfilament integrity,and mitotic activity in cultured human fibroblasts and HeLa cells

Summary Human fibroblasts and HeLa cells were treated with bunaftine (N-butyl-N-/2-(diethylamino)ethyl/-1-naphthalenecarboxamide) in vitro. At concentrations of 0.5–2.0 mM, the drug caused contraction and rounding of the cells with loss of microvilli-like processes. Aggregates of dense, partly granular, partly fibrillar material formed in the cytoplasm and the rough endoplasmic reticulum became vesiculated. Immunofiuorescence microscopy with DNase I and anti-DNase I demonstrated that bundles of actin filaments were disrupted, forming rings, coils, and granules. Filaments stained with antibodies to vimentin (fibroblasts) and prekeratin (HeLa cells) showed less characteristic rearrangements, probably related to the rounding up of the cells. 0.4 mM bunaftine increased and 0.8–1.0 mM markedly decreased the percentage of mitotic cells, without accumulation of cells in any particular stage of mitosis. The drug may arrest the cell cycle at some point before mitosis; it may have a critical concentration above which the arrest becomes permanent.These results suggest that bunaftine interferes with the integrity of microfilament bundles in a different manner from that of cytochalasins. It does not cause any depletion of cellular ATP, indicating that its effect is not a result of inhibition of cell metabolism. It is proposed that bunaftine may be used as a complement to cytochalasins in studies of the microfilament system of the cell. The possible binding of bunaftine to actin or myosin and further details of its mechanism of action remain to be elucidated.     

Anencephaly in trisomy 18 associated with elevated alpha-1-fetoprotein in amniotic fluid

Summary Elevated levels of alpha-1-fetoprotein (AFP) were found in the amniotic fluid of a 36-year-old woman in the 15th week of gestation. Because of this and the results of repeated ultrasonography, abortion was induced. An anencephalic fetus with trisomy 18 was delivered. The possible correlation among neural-tube defects, chromosomal abnormalities, and level of AFP is discussed.