Oligarchies in Amazonian tree communities: a ten‐year review

This paper revisits various hypotheses about oligarchic patterns in Amazonian tree communities put forward by Pitman et al. (2001) . Together, these hypotheses predict that most lowland sites in the Amazon are located within large patches of relatively homogeneous edaphic and other environmental conditions, where an oligarchy of common, frequent tree species accounts for a majority of trees. To assess the degree to which these hypotheses have been corroborated or refuted over the last ten years, we reviewed > 200 studies published since 2001. We found overwhelming support for the hypo thesis that large‐scale oligarchies of common and frequent species are a common feature of Amazonian tree communities. At least 22 studies have documented oligarchies in Amazonian woody plant communities to date, and no studies have looked for oligarchies as defined by Pitman et al. (2001) and failed to find them. We argue that six publications that offer critiques of the oligarchy hypothesis do not constitute valid tests. The other hypotheses in Pitman et al. (2001) – one regarding the specific oligarchic taxa that dominate forests near the eastern base of the Andes and one that attempts to explain why oligarchic species exist – are less well supported by the literature, in large part because they have not been subjected to many tests. We discuss links between these hypotheses and other well‐known patterns and hypotheses in ecology (the abundance–occupancy relationship, the Janzen–Connell hypothesis, the niche‐environment hypothesis, and the niche breadth hypothesis), and provide additional detail to facilitate rigorous tests in the future. The paper concludes by presenting remote sensing evidence that large patches of relatively homogeneous environmental conditions account for most of the upland forest landscape across Amazonian Peru.     

ADP-ribosylation of glutamine synthetase in the cyanobacterium Synechocystis sp. strain PCC 6803.

Glutamine synthetase (GS) inactivation was observed in crude cell extracts and in the high-speed supernatant fraction from the cyanobacterium Synechocystis sp. strain PCC 6803 following the addition of ammonium ions, glutamine, or glutamate. Dialysis of the high-speed supernatant resulted in loss of inactivation activity, but this could be restored by the addition of NADH, NADPH, or NADP+ and, to a lesser extent, NAD+, suggesting that inactivation of GS involved ADP-ribosylation. This form of modification was confirmed both by labelling experiments using [32P]NAD+ and by chemical analysis of the hydrolyzed enzyme. Three different forms of GS, exhibiting no activity, biosynthetic activity only, or transferase activity only, could be resolved by chromatography, and the differences in activity were correlated with the extent of the modification. Both biosynthetic and transferase activities were restored to the completely inactive form of GS by treatment with phosphodiesterase.     

X-ray structure of human acid-beta-glucosidase covalently bound to conduritol-B-epoxide. Implications for Gaucher disease

Gaucher disease is an inherited metabolic disorder caused by mutations in the lysosomal enzyme acid-beta-glucosidase (GlcCerase). We recently determined the x-ray structure of GlcCerase to 2.0 A resolution (Dvir, H., Harel, M., McCarthy, A. A., Toker, L., Silman, I., Futerman, A. H., and Sussman, J. L. (2003) EMBO Rep.4, 704-709) and have now solved the structure of Glc-Cerase conjugated with an irreversible inhibitor, conduritol-B-epoxide (CBE). The crystal structure reveals that binding of CBE to the active site does not induce a global conformational change in GlcCerase and confirms that Glu340 is the catalytic nucleophile. However, only one of two alternative conformations of a pair of flexible loops (residues 345-349 and 394-399) located at the entrance to the active site in native GlcCerase is observed in the GlcCerase-CBE structure, a conformation in which the active site is accessible to CBE. Analysis of the dynamics of these two alternative conformations suggests that the two loops act as a lid at the entrance to the active site. This possibility is supported by a cluster of mutations in loop 394-399 that cause Gaucher disease by reducing catalytic activity. Moreover, in silico mutational analysis demonstrates that all these mutations stabilize the conformation that limits access to the active site, thus providing a mechanistic explanation of how mutations in this loop result in Gaucher disease.     

DEVELOPMENTAL CHANGES IN LEVELS AND FORMS OF CHOLINESTERASES IN MUSCLES OF NORMAL AND DYSTROPHIC CHICKENS

Abstract— Acetylcholinesterase (AChE) and pseudocholinesterase (°ChE) were studied in vivo and during the first several months of development of pectoral and posterior latissimi dorsi (PLD) muscles in normal and dystrophic chickens. Muscle extracts were prepared in a high ionic strength-nonionic detergent medium in the presence of protease inhibitors, in order to obtain complete solubilization and to prevent degradation of intrinsic molecular forms of both enzymes. In both normal and dystrophic pectoral muscles levels of AChE and °ChE increase rapidly in vivo, °ChE accounting for 5–10% of total cholinesterase activity. In the normal pectoral muscle the concentration of both enzymes drops rapidly after hatching with increasing muscle mass; total AChE per muscle remains relatively constant for 30 days post-hatch. In the dystrophic pectoral muscle both AChE and °ChE accumulate after hatching, resulting in greatly elevated levels (approx 10–25-fold) of both enzymes throughout the period studied. Multiple molecular forms of AChE and °ChE are observed in the pectoral muscle by sucrose gradient centrifugation. Four principal forms are distinguished: two light (L₁, L₂), one medium (M), and one heavy (H₂). The °ChE forms are 0.5–1.0 S units lighter than the corresponding AChE forms. L₂ is the predominant light form of AChE, whereas L₁ is the major light °ChE form detected. The lighter forms of AChE predominate in normal and dystrophic embryonic pectoral muscle at day 14, being replaced by the H₂ form by day 19. H₂ is the major °ChE form detected at day 19. After hatching, H₂ AChE is the predominant form found in both of the normal muscles studied. In the dystrophic pectoral muscle, progressive accumulation of the L₂ form of AChE is detected as early as day 4 post-hatch; this form eventually becomes predominant, although the heavier forms are also elevated. In PLD muscle the same phenomenon occurs, but with a slower time course. In dystrophic pectoral muscle a similar rise in the L₁ form of °ChE is first observed by day 4, with heavier forms also elevated in the mature muscle. Thus the alteration in the control of these two enzymes in dystrophic fast-twitch muscles results in an accumulation of the light forms of AChE and °ChE.     

Whole-genome scan, in a complex disease, using 11,245 single-nucleotide polymorphisms: comparison with microsatellites

Despite the theoretical evidence of the utility of single-nucleotide polymorphisms (SNPs) for linkage analysis, no whole-genome scans of a complex disease have yet been published to directly compare SNPs with microsatellites. Here, we describe a whole-genome screen of 157 families with multiple cases of rheumatoid arthritis (RA), performed using 11,245 genomewide SNPs. The results were compared with those from a 10-cM microsatellite scan in the same cohort. The SNP analysis detected HLA*DRB1, the major RA susceptibility locus (P=.00004), with a linkage interval of 31 cM, compared with a 50-cM linkage interval detected by the microsatellite scan. In addition, four loci were detected at a nominal significance level (P<.05) in the SNP linkage analysis; these were not observed in the microsatellite scan. We demonstrate that variation in information content was the main factor contributing to observed differences in the two scans, with the SNPs providing significantly higher information content than the microsatellites. Reducing the number of SNPs in the marker set to 3,300 (1-cM spacing) caused several loci to drop below nominal significance levels, suggesting that decreases in information content can have significant effects on linkage results. In contrast, differences in maps employed in the analysis, the low detectable rate of genotyping error, and the presence of moderate linkage disequilibrium between markers did not significantly affect the results. We have demonstrated the utility of a dense SNP map for performing linkage analysis in a late-age-at-onset disease, where DNA from parents is not always available. The high SNP density allows loci to be defined more precisely and provides a partial scaffold for association studies, substantially reducing the resource requirement for gene-mapping studies.     

Keep collecting: accurate species distribution modelling requires more collections than previously thought

Aim Species distribution models (SDMs) use the locations of collection records to map the distributions of species, making them a powerful tool in conservation biology, ecology and biogeography. However, the accuracy of range predictions may be reduced by temporally autocorrelated biases in the data. We assess the accuracy of SDMs in predicting the ranges of tropical plant species on the basis of different sample sizes while incorporating real‐world collection patterns and biases. Location Tropical South American moist forests. Methods We use dated herbarium records to model the distributions of 65 Amazonian and Andean plant species. For each species, we use the first 25, 50, 100, 125 and 150 records collected and available for each species to analyse changes in spatial aggregation and climatic representativeness through time. We compare the accuracy of SDM range estimates produced using the time‐ordered data subsets to the accuracy of range estimates generated using the same number of collections but randomly subsampled from all available records. Results We find that collections become increasingly aggregated through time but that additional collecting sites are added resulting in progressively better representations of the species’ full climatic niches. The range predictions produced using time‐ordered data subsets are less accurate than predictions from random subsets of equal sample sizes. Range predictions produced using time‐ordered data subsets consistently underestimate the extent of ranges while no such tendency exists for range predictions produced using random data subsets. Main conclusions These results suggest that larger sample sizes are required to accurately map species ranges. Additional attention should be given to increasing the number of records available per species through continued collecting, better distributed collecting, and/or increasing access to existing collections. The fact that SDMs generally under‐predict the extent of species ranges means that extinction risks of species because of future habitat loss may be lower than previously estimated.     

A structural motif of acetylcholinesterase that promotes amyloid beta-peptide fibril formation

Acetylcholinesterase (AChE) has been found to be associated with the core of senile plaques. We have shown that AChE interacts with the amyloid beta-peptide (Abeta) and promotes amyloid fibril formation by a hydrophobic environment close to the peripheral anionic binding site (PAS) of the enzyme. Here we present evidence for the structural motif of AChE involved in this interaction. First, we modeled the docking of Abeta onto the structure of Torpedo californica AChE, and identified four potential sites for AChE-Abeta complex formation. One of these, Site I, spans a major hydrophobic sequence exposed on the surface of AChE, which had been previously shown to interact with liposomes [Shin et al. (1996) Protein Sci. 5, 42-51]. Second, we examined several AChE-derived peptides and found that a synthetic 35-residue peptide corresponding to the above hydrophobic sequence was able to promote amyloid formation. We also studied the ability to promote amyloid formation of two synthetic 24-residue peptides derived from the sequence of a Omega-loop, which has been suggested as an AChE-Abeta interacting motif. Kinetic analyses indicate that only the 35-residue hydrophobic peptide mimics the effect of intact AChE on amyloid formation. Moreover, RP-HPLC analysis revealed that the 35-residue peptide was incorporated into the growing Abeta-fibrils. Finally, fluorescence binding studies showed that this peptide binds Abeta with a K(d) = 184 microM, independent of salt concentration, indicating that the interaction is primarily hydrophobic. Our results indicate that the homologous human AChE motif is capable of accelerating Abeta fibrillogenesis.