Pathways of soil genesis in the Coast Range of Oregon, USA

Background and Aims

Soil chronosequences on marine terraces along the Pacific Coast of California and Oregon show evidence of podzolization, though soils ultimately evolve to Ultisols. It is not clear if this pathway of soil evolution can be extended to the humid, inland Oregon Coast Range.

Methods

We analyzed soil properties for a fluvial terrace chronosequence sampled along the Siuslaw River (Oregon, USA) about 50 km from the Pacific coast. The seven terraces ranged in age from <3.5 ky to nearly 1,000 ky.

Results

There was no evidence of early podsolization. Instead, evidence was found that andisolization starts early and occurs even in older soils when pedogenic iron accumulation and clay synthesis and illuviation dominate. Soils develop the morphology characteristic of Ultisols sometime between 20 and 70 ky, but high levels of oxalate extractable iron and aluminum satisfy criteria of an andic subgroup. Alfisols are not formed as an intermediary stage.

Conclusions

The lack of Spodosols inland is due to the inland shift from udic to ustic or xeric moisture regime, which favors summer drying and ripening of short-range order minerals rather than deep leaching or translocation. Other factors are higher pH, different organic chemistry and faster calcium cycling under the Douglas fir inland when compared to the Sitka spruce of the coastal terraces.     

“Prey Play”: Learning about Predators and Prey through an Interactive,Role-Play Game

“Prey Play” is an interactive role-play activity that provides fifth-grade students with opportunities to examine predator–prey interactions. This four-part, role-play activity allows students to take on the role of a predator and prey as they reflect on the behaviors animals exhibit as they collect food and interact with one another, as well as limiting factors. Through this activity, students will enhance their communication and observation skills and showcase their creativity.     

Compensatory Hemagglutinin Mutations Alter Antigenic Properties of Influenza Viruses

Influenza viruses routinely acquire mutations in antigenic sites on the globular head of the hemagglutinin (HA) protein. Since these antigenic sites are near the receptor binding pocket of HA, many antigenic mutations simultaneously alter the receptor binding properties of HA. We previously reported that a K165E mutation in the Sa antigenic site of A/Puerto Rico/8/34 (PR8) HA is associated with secondary neuraminidase (NA) mutations that decrease NA activity. Here, using reverse genetics, we show that the K165E HA mutation dramatically decreases HA binding to sialic acid receptors on cell surfaces. We sequentially passaged reverse-genetics-derived PR8 viruses with the K165E antigenic HA mutation in fertilized chicken eggs, and to our surprise, viruses with secondary NA mutations did not emerge. Instead, viruses with secondary HA mutations emerged in 3 independent passaging experiments, and each of these mutations increased HA binding to sialic acid receptors. Importantly, these compensatory HA mutations were located in the Ca antigenic site and prevented binding of Ca-specific monoclonal antibodies. Taken together, these data indicate that HA antigenic mutations that alter receptor binding avidity can be compensated for by secondary HA or NA mutations. Antigenic diversification of influenza viruses can therefore occur irrespective of direct antibody pressure, since compensatory HA mutations can be located in distinct antibody binding sites.     

Interaction of p190RhoGAP with C-terminal Domain of p120-catenin Modulates Endothelial Cytoskeleton and Permeability

p120-catenin is a multidomain intracellular protein, which mediates a number of cellular functions, including stabilization of cell-cell transmembrane cadherin complexes as well as regulation of actin dynamics associated with barrier function, lamellipodia formation, and cell migration via modulation of the activities of small GTPAses. One mechanism involves p120 catenin interaction with Rho GTPase activating protein (p190RhoGAP), leading to p190RhoGAP recruitment to cell periphery and local inhibition of Rho activity. In this study, we have identified a stretch of 23 amino acids within the C-terminal domain of p120 catenin as the minimal sequence responsible for the recruitment of p190RhoGAP (herein referred to as CRAD; catenin-RhoGAP association domain). Expression of the p120-catenin truncated mutant lacking the CRAD in endothelial cells attenuated effects of barrier protective oxidized phospholipid, OxPAPC. This effect was accompanied by inhibition of membrane translocation of p190RhoGAP, increased Rho signaling, as well as suppressed activation of Rac1 and its cytoskeletal effectors PAK1 (p21-activated kinase 1) and cortactin. Expression of p120 catenin-truncated mutant lacking CRAD also delayed the recovery process after thrombin-induced endothelial barrier disruption. Concomitantly, RhoA activation and downstream signaling were sustained for a longer period of time, whereas Rac signaling was inhibited. These data demonstrate a critical role for p120-catenin (amino acids 820–843) domain in the p120-catenin·p190RhoGAP signaling complex assembly, membrane targeting, and stimulation of p190RhoGAP activity toward inhibition of the Rho pathway and reciprocal up-regulation of Rac signaling critical for endothelial barrier regulation.     

Fatty acid remodeling in cellular glycerophospholipids following the activation of human T cells

Changes in fatty acid (FA) and glycerophospholipid (GPL) metabolism associated with cell cycle entry are not fully understood. In this study FA-GPL remodeling was investigated in resting and proliferating primary human T cells. Significant changes were measured in the composition and distribution of FAs in GPLs following receptor activation of human T cells. The FA distribution of proliferating T cells was very similar to that of the human Jurkat T cell line and when the stimulus was removed from proliferating T cells, they stopped proliferating and the FA distribution largely reverted back to that of resting T cells. The cellular content of saturated and monounsaturated FAs was significantly increased in proliferating cells, which was associated with an induction of FA synthase and stearoyl-CoA desaturase-1 gene expression. Additionally, cellular arachidonate was redistributed in GPLs in a distinct pattern that was unlike any other FAs. This redistribution was associated with an induction of CoA-dependent and CoA-independent remodeling. Accordingly, significant changes in the expression of several acyl-CoA synthetases, lysophospholipid acyltransferases, and phospholipase A₂ were measured. Overall, these results suggest that metabolic pathways are activated in proliferating T cells that may represent fundamental changes associated with human cell proliferation.     

Identification of Biochemically Distinct Properties of the Small Ubiquitin-related Modifier (SUMO) Conjugation Pathway in Plasmodium falciparum

Small ubiquitin-related modifiers (SUMOs) are post-translationally conjugated to other proteins and are thereby essential regulators of a wide range of cellular processes. Sumoylation, and enzymes of the sumoylation pathway, are conserved in the malaria causing parasite, Plasmodium falciparum. However, the specific functions of sumoylation in P. falciparum, and the degree of functional conservation between enzymes of the human and P. falciparum sumoylation pathways, have not been characterized. Here, we demonstrate that sumoylation levels peak during midstages of the intra-erythrocyte developmental cycle, concomitant with hemoglobin consumption and elevated oxidative stress. In vitro studies revealed that P. falciparum E1- and E2-conjugating enzymes interact effectively to recognize and modify RanGAP1, a model mammalian SUMO substrate. However, in heterologous reactions, P. falciparum E1 and E2 enzymes failed to interact with cognate human E2 and E1 partners, respectively, to modify RanGAP1. Structural analysis, binding studies, and functional assays revealed divergent amino acid residues within the E1-E2 binding interface that define organism-specific enzyme interactions. Our studies identify sumoylation as a potentially important regulator of oxidative stress response during the P. falciparum intra-erythrocyte developmental cycle, and define E1 and E2 interactions as a promising target for development of parasite-specific inhibitors of sumoylation and parasite replication.     

The influence of goethite and gibbsite on soluble nutrient dynamics and microbial community composition

Iron and aluminum (oxyhydr)oxides are ubiquitous in the soil environment and have the potential to strongly affect the properties of dissolved organic matter. We examined the effect of oxide surfaces on soluble nutrient dynamics and microbial community composition using an incubation of forest floor material in the presence of (1) goethite and quartz, (2) gibbsite and quartz, and (3) quartz surfaces. Forest floor material was incubated over a period of 154 days. Aqueous extracts of the incubations were harvested on days 5, 10, 20, 30, 60, 90, and 154, and concentrations of P, N, PO₄ ^3?, NO₂ ^?, NO₃ ^?, and organic C were measured in the solutions. Microbial community composition was examined through pyrosequencing of bacterial and fungal small subunit ribosomal RNA genes on selected dates throughout the incubation. Results indicated that oxide surfaces exerted strong control on soluble nutrient dynamics and on the composition of the decomposer microbial community, while possibly having a small impact on system-level respiration. Goethite and gibbsite surfaces showed preferential adsorption of P-containing and high molar mass organic solutes, but not of N-containing compounds. On average, organic C concentrations were significantly lower in water extractable organic matter (WEOM) solutions from oxide treatments than from the control treatment (P = 0.0037). Microbial community composition varied both among treatments and with increasing time of incubation. Variation in bacterial and fungal community composition exhibited strong-to-moderate correlation with length of incubation, and several WEOM physiochemical characteristics including apparent (weight averaged) molar mass, pH and electrical conductivity. Additionally, variation in bacterial community composition among treatments was correlated with total P (r = 0.60, P < 0.0001), PO₄ ^3? (r = 0.79, P < 0.0001), and organic C (r = 0.36, P = 0.015) concentrations; while variation in fungal communities was correlated with organic C concentrations (r = ?0.48, P = 0.0008) but not with phosphorus concentrations. The relatively small impact of oxide surfaces on system-level microbial respiration of organic matter despite their significant effects on microbial community composition and WEOM dynamics lends additional support to the theory of microbial functional redundancy.     

VACCINATION AND REDUCED COHORT DURATION CAN DRIVE VIRULENCE EVOLUTION: MAREK’S DISEASE VIRUS AND INDUSTRIALIZED AGRICULTURE

Marek’s disease virus (MDV), a commercially important disease of poultry, has become substantially more virulent over the last 60 years. This evolution was presumably a consequence of changes in virus ecology associated with the intensification of the poultry industry. Here, we assess whether vaccination or reduced host life span could have generated natural selection, which favored more virulent strains. Using previously published experimental data, we estimated viral fitness under a range of cohort durations and vaccine treatments on broiler farms. We found that viral fitness maximized at intermediate virulence, as a result of a trade‐off between virulence and transmission previously reported. Our results suggest that vaccination, acting on this trade‐off, could have led to the evolution of increased virulence. By keeping the host alive, vaccination prolongs infectious periods of virulent strains. Improvements in host genetics and nutrition, which reduced broiler life spans below 50 days, could have also increased the virulence of the circulating MDV strains because shortened cohort duration reduces the impact of host death on viral fitness. These results illustrate the dramatic impact anthropogenic change can potentially have on pathogen virulence.