A comparative measure of biodiversity based on species composition

In conservation planning, species richness and species endemism are the most often used metrics for describing the biodiversity importance of areas. However, when it comes to prioritizing regions for conservation actions these measures alone are insufficient because they do not reveal how similar or different the actual composition of species may be from one area to another. For comparative analysis an additional useful metric would be one that indicates the degree to which the species assemblage in one area is also represented in—or is distinct from—species assemblages of other areas. Here we describe a method for quantifying the compositional representativeness of species assemblages among geographic regions. The method generates asymmetric pairwise similarity coefficients that are then used to calculate separate measures for the representativeness and the distinctiveness of species assemblages in the regions being compared. We demonstrate the method by comparing fish communities among freshwater ecoregions of the Mississippi Basin, and then among smaller hydrological units within two individual freshwater ecoregions. At both scales of analysis, our measures of representativeness and distinctiveness reveal patterns of fish species composition that differ from patterns of species richness. This information can enhance conservation planning processes by ensuring that priority-setting explicitly consider the most representative and distinctive species assemblages.     

Immunisation with recombinant PfEMP1 domains elicits functional rosette-inhibiting and phagocytosis-inducing antibodies to Plasmodium falciparum

Background

Rosetting is a Plasmodium falciparum virulence factor implicated in the pathogenesis of life-threatening malaria. Rosetting occurs when parasite–derived P. falciparum Erythrocyte Membrane Protein One (PfEMP1) on the surface of infected erythrocytes binds to human receptors on uninfected erythrocytes. PfEMP1 is a possible target for a vaccine to induce antibodies to inhibit rosetting and prevent severe malaria.

Methodology/Findings

We examined the vaccine potential of the six extracellular domains of a rosette-mediating PfEMP1 variant (ITvar9/R29var1 from the R29 parasite strain) by immunizing rabbits with recombinant proteins expressed in E. coli. Antibodies raised to each domain were tested for surface fluorescence with live infected erythrocytes, rosette inhibition and phagocytosis-induction. Antibodies to all PfEMP1 domains recognized the surface of live infected erythrocytes down to low concentrations (0.02–1.56 µg/ml of total IgG). Antibodies to all PfEMP1 domains except for the second Duffy-Binding-Like region inhibited rosetting (50% inhibitory concentration 0.04–4 µg/ml) and were able to opsonize and induce phagocytosis of infected erythrocytes at low concentrations (1.56–6.25 µg/ml). Antibodies to the N-terminal region (NTS-DBL1α) were the most effective in all assays. All antibodies were specific for the R29 parasite strain, and showed no functional activity against five other rosetting strains.

Conclusions/Significance

These results are encouraging for vaccine development as they show that potent antibodies can be generated to recombinant PfEMP1 domains that will inhibit rosetting and induce phagocytosis of infected erythrocytes. However, further work is needed on rosetting mechanisms and cross-reactivity in field isolates to define a set of PfEMP1 variants that could induce functional antibodies against a broad range of P. falciparum rosetting parasites.     

Metapopulation extinction risk: Dispersal’s duplicity

Metapopulation extinction risk is the probability that all local populations are simultaneously extinct during a fixed time frame. Dispersal may reduce a metapopulation’s extinction risk by raising its average per-capita growth rate. By contrast, dispersal may raise a metapopulation’s extinction risk by reducing its average population density. Which effect prevails is controlled by habitat fragmentation. Dispersal in mildly fragmented habitat reduces a metapopulation’s extinction risk by raising its average per-capita growth rate without causing any appreciable drop in its average population density. By contrast, dispersal in severely fragmented habitat raises a metapopulation’s extinction risk because the rise in its average per-capita growth rate is more than offset by the decline in its average population density. The metapopulation model used here shows several other interesting phenomena. Dispersal in sufficiently fragmented habitat reduces a metapopulation’s extinction risk to that of a constant environment. Dispersal between habitat fragments reduces a metapopulation’s extinction risk insofar as local environments are asynchronous. Grouped dispersal raises the effective habitat fragmentation level. Dispersal search barriers raise metapopulation extinction risk. Nonuniform dispersal may reduce the effective fraction of suitable habitat fragments below the extinction threshold. Nonuniform dispersal may make demographic stochasticity a more potent metapopulation extinction force than environmental stochasticity.     

Pathways of Anaerobic Acetate Utilization in Escherichia coli and Aerobacter cloacae

Acetate-1-¹⁴C was added to anaerobic glucose-fermenting cultures of Escherichia coli and Aerobacter cloacae. In the E. coli culture, lactate formation occurred late in the fermentation, when the rate of production of formate and acetate had decreased. The occurrence of acetate label in the lactate indicated formation of pyruvate from acetyl-coenzyme A (CoA) and formate. In the A. cloacae cultures, substantial amounts of acetate label were found in the 2,3-butanediol formed. Evidence is presented that the label could have entered the diol only by conversion of formate and acetyl-CoA into pyruvate. The observed levels of radioactivity in the diol indicated that during diol formation the reaction yielding formate and acetyl-CoA from pyruvate CoA was operating close to equilibrium. The shift in metabolism from formation of acetate, ethyl alcohol, and formate to the formation of butanediol or lactate appears to be due basically to an approach to equilibrium of the pyruvate-splitting reaction, whatever the induction mechanism by which the shift is implemented.     

Packaging Specific Segments of the Salmonella Chromosome with Locked-in Mud-P22 Prophages

Hybrid genetic elements, Mud-P and Mud-Q (collectively, Mud-P22s), have been constructed that carry two-thirds of the temperate Salmonella phage P22 genome sandwiched between the ends of transposon Mu. Insertions of these elements in the Salmonella chromosome generate locked-in P22 prophages that cannot excise. Upon induction (as a consequence of the inactivation of P22 c2 repressor), a locked-in prophage replicates its DNA in situ, resulting in the amplification of neighboring regions of the chromosome and the processive packaging of three contiguous headsful of adjacent DNA in one direction from the P22 packaging site, pac. Phage particles in an induced lysate of a Mud-P22 lysogen contain DNA molecules corresponding to several minutes of chromosomal DNA adjacent to the site of prophage insertion and transduce nearby genetic markers with high efficiencies. Mud-P22 prophages have been introduced into an F' episome by transposition; resident Mud insertions on the Salmonella chromosome may be converted to Mud-P22 insertions by homologous recombination in P22-mediated transductional crosses.     

Facial Morphogenesis of the Earliest Europeans

The modern human face differs from that of our early ancestors in that the facial profile is relatively retracted (orthognathic). This change in facial profile is associated with a characteristic spatial distribution of bone deposition and resorption: growth remodeling. For humans, surface resorption commonly dominates on anteriorly-facing areas of the subnasal region of the maxilla and mandible during development. We mapped the distribution of facial growth remodeling activities on the 900–800 ky maxilla ATD6-69 assigned to H. antecessor, and on the 1.5 My cranium KNM-WT 15000, part of an associated skeleton assigned to African H. erectus. We show that, as in H. sapiens, H. antecessor shows bone resorption over most of the subnasal region. This pattern contrasts with that seen in KNM-WT 15000 where evidence of bone deposition, not resorption, was identified. KNM-WT 15000 is similar to Australopithecus and the extant African apes in this localized area of bone deposition. These new data point to diversity of patterns of facial growth in fossil Homo. The similarities in facial growth in H. antecessor and H. sapiens suggest that one key developmental change responsible for the characteristic facial morphology of modern humans can be traced back at least to H. antecessor.     

Inhibition of ROCK activity allows InlF-mediated invasion and increased virulence of Listeria monocytogenes

Listeria monocytogenes is an intracellular bacterial pathogen that causes life-threatening disease. The mechanisms used by L. monocytogenes to invade non-professional phagocytic cells are not fully understood. In addition to the requirement of bacterial determinants, host cell conditions profoundly influence infection. Here, we have shown that inhibition of the RhoA/ROCK pathway by pharmacological inhibitors or RNA interference results in increased L. monocytogenes invasion of murine fibroblasts and hepatocytes. InlF, a member of the internalin multigene family with no known function, was identified as a L. monocytogenes -specific factor mediating increased host cell binding and entry. Conversely, activation of RhoA/ROCK activity resulted in decreased L. monocytogenes adhesion and invasion. Furthermore, virulence of wild-type bacteria during infection of mice was significantly increased upon inhibition of ROCK activity, whereas colonization and virulence of an inlF deletion mutant was not affected, thus supporting a role for InlF as a functional virulence determinant in vivo under specific conditions. In addition, inhibition of ROCK activity in human-derived cells enhanced either bacterial adhesion or adhesion and entry in an InlF-independent manner, further suggesting a host species or cell type-specific role for InlF and that additional bacterial determinants are involved in mediating ROCK-regulated invasion of human cells.     

Spontaneous and nitrosourea-induced primary tumors of the central nervous system in Fischer 344 rats chronically exposed to 836 MHz modulated microwaves.

We have tested an 836.55 MHz field with North American Digital Cellular (NADC) modulation in a 2-year animal bioassay that included fetal exposure. In offspring of pregnant Fischer 344 rats, we tested both spontaneous tumorigenicity and the incidence of induced central nervous system (CNS) tumors after a single dose of the carcinogen ethylnitrosourea (ENU) in utero, followed by intermittent digital-phone field exposure for 24 months. Far-field exposures began on gestational day 19 and continued until weaning at age 21 days. Near-field exposures began at 35 days and continued for the next 22 months, 4 consecutive days weekly, 2 h/day. SAR levels simulated localized peak brain exposures of a cell phone user. Of the 236 original rats, 182 (77%) survived to the termination of the whole experiment and were sacrificed at age 709-712 days. The 54 rats (23%) that died during the study ("preterm rats") formed a separate group for some statistical analyses. There was no evidence of tumorigenic effects in the CNS from exposure to the TDMA field. However, some evidence of tumor-inhibiting effects of TDMA exposure was apparent. Overall, the TDMA field-exposed animals exhibited trends toward a reduced incidence of spontaneous CNS tumors (P < 0. 16, two-tailed) and ENU-induced CNS tumors (P < 0.16, two-tailed). In preterm rats, where primary neural tumors were determined to be the cause of death, fields decreased the incidence of ENU-induced tumors (P < 0.03, two-tailed). We discuss a possible approach to evaluating with greater certainty the possible inhibitory effects of TDMA-field exposure on tumorigenesis in the CNS.