Predation risks suppress lifetime fitness in a wild mammal

Prey often reduce predation risk at the cost of lower resource intake. The cumulative effects of such tradeoffs can alter resource allocation, demography and evolutionary processes. We show how the accumulation of risk effects reduces the growth rate of wild North American porcupines Erethizon dorsatum, and simulate three evolutionary responses related to lifetime reproductive success. Individual porcupines experiencing predation risk from fishers Pekania pennanti grew slower and gave birth to fewer offspring. Simulations show that predation risk alone can lead to population declines, and that a female can replace herself by investing more energy into reproduction or adult survival; females that only invest energy in juvenile survival cannot. We show that the accumulation of predation risk can reduce lifetime reproductive success in natural ecosystems. Estimating the contribution of predation risk, and how evolutionary responses can mediate consequences associated with predation risk, is necessary to understand the evolution of predator–prey systems.     

Predicting the occurrence of host-associated differentiation in parasitic arthropods: a quantitative literature review

Parasite populations associated with different host species can encounter a variety of isolating reproductive barriers, leading to each population independently accumulating genome-wide genetic differences due to their host associations. This phenomenon is called host-associated differentiation (HAD) and has been proposed as an indicator of early diversification among parasitic arthropods. Although many parasite–host case study systems have been tested for the genetic signature of HAD (e.g., F_ST≥0.15 between sympatric, host-associated populations in the absence of allopatry), it is unknown which isolating reproductive barriers best predict the general occurrence of HAD. HAD development has been attributed to biological and ecological factors that either directly generate reproductive isolation between parasites living on different hosts, such as ‘immigrant inviability’ (i.e., lower fitness of immigrants in non-native environments), or that promote the accumulation of host-specific genetic adaptations, such as the gallmaking feeding mode. In fact, some of these factors are shared across multiple case studies, suggesting that the occurrence of HAD is generalizable and can be predicted based on the incidence of significant biological and ecological factors. By means of a discriminant function analysis (DFA), this research assessed 108 arthropod parasite–host case studies for ecological and biological factors significantly correlated with the occurrence of HAD and whether these factors could be used to distinguish the presence of HAD from its absence. The DFA demonstrated that case studies that developed HAD could be distinguished from case studies that did not develop HAD. The results of the DFA were corroborated by a ‘non-iterative partial least squares’ (NIPALS) discriminant model and a nominal logistic regression. Case studies with HAD could be robustly separated from case studies without HAD based on the incidence of these predictive factors: immigrant inviability, gallmaking, endophagy, recent range invasions of either hosts or parasites, differential host phenology, and differential parasite morphology. These results were used in an infinite random forest analysis to generate a hierarchy of conditional probabilities that separated HAD presence from absence. The results provide researchers with a tool for reliably predicting which untested parasite–host system would likely develop HAD. Immigrant inviability, gallmaking, and their combination were strongly correlated with the presence of HAD, which indicated parasite–host systems with these traits were highly likely to develop HAD. Contrary to expectation, endophagous feeding was negatively correlated with HAD presence, which indicated phytophagous endophagous feeders (excepting gallmakers) were highly unlikely to develop HAD. Furthermore, parasitoids were shown to be just as likely to develop HAD as not. Unfortunately, potentially significant predictive factors (e.g., allochrony) were excluded from analysis because too few case studies have been specifically tested for these factors. Furthermore, this analysis was biased by the lack of ‘negative’ publication results and the overrepresentation of research laboratories that primarily study HAD. Future research should accumulate novel HAD case studies that specifically test for allochrony, differential microbial associations, and morphological differentiation.     

Purification and characterization of the human recombinant histidine-tagged prostaglandin endoperoxide H synthases-1 and -2

We have used in vitro mutagenesis to introduce a six residue histidine sequence (His-tag) near the amino terminal end of the human PGHS-1 and -2 and have expressed these proteins using the baculovirus system. The His-tags are located one and two amino acids beyond the signal peptide cleavage sites of PGHS-1 and PGHS-2, respectively, positions that do not affect their activities or sensitivities to nonsteroidal anti-inflammatory drugs. When expressed in sf-21 cells, the His-tagged enzymes have K(m) values for arachidonate, and IC(50) values for inhibition by nonsteroidal anti-inflammatory drugs that are similar to values reported for the nontagged enzymes. The His-tags allowed for purification of the PGHSs by a simplified protocol involving nickel-affinity and anion exchange FPLC chromatography. The specific activities and recoveries for the purified enzymes were as good or better than those reported previously for purification of the non-tagged PGHS. These baculovirus constructs should provide a convenient source for pharmacologic and biophysical studies that require large scale preparation of human PGHSs.     

Nanoparticle Surface-Enhanced Raman Scattering of Bacteriorhodopsin Stabilized by Amphipol A8-35

Surface-enhanced Raman spectroscopy (SERS) has developed dramatically since its discovery in the 1970s, because of its power as an analytical tool for selective sensing of molecules adsorbed onto noble metal nanoparticles (NPs) and nanostructures, including at the single-molecule (SM) level. Despite the high importance of membrane proteins (MPs), SERS application to MPs has not really been studied, due to the great handling difficulties resulting from the amphiphilic nature of MPs. The ability of amphipols (APols) to trap MPs and keep them soluble, stable, and functional opens up onto highly interesting applications for SERS studies, possibly at the SM level. This seems to be feasible since single APol-trapped MPs can fit into gaps between noble metal NPs, or in other gap-containing SERS substrates, whereby the enhancement of Raman scattering signal may be sufficient for SM sensitivity. The goal of the present study is to give a proof of concept of SERS with APol-stabilized MPs, using bacteriorhodopsin (BR) as a model. BR trapped by APol A8-35 remains functional even after partial drying at a low humidity. A dried mixture of silver Lee–Meisel colloid NPs and BR/A8-35 complexes give rise to SERS with an average enhancement factor in excess of 10². SERS spectra resemble non-SERS spectra of a dried sample of BR/APol complexes.     

Prenatal detection of an unstable ring 21 chromosome

Summary An unstable ring chromosome 21 detected through prenatal studies was associated at birth with an apparently normal male phenotype. At 14 months of age, examination indicated only minor developmental delay. The majority of cells examined from amniocyte, fibroblast, and lymphocyte cultures contained an asymmetrical dicentric ring 21 chromosome which was larger than a normal chromosome 21. This ring is presumed to be a duplication for most of chromosome 21 and a deletion of part of the terminal regions. The karyotype is described as mos45, XY,-21/46,XY,r(21)(p13q22.3). The child is monosomic for part of the sub-band 21q22.3 in every cell and trisomic for the remainder of the chromosome in most of his cells. The terminal deletion does not appear to have been severely detrimental to the phenotype and the effective trisomy present in many cells studies was insufficient to cause the Down syndrome.     

Mouse Virulence of K(L) Antigen-Containing Strains of Escherichia coli

The mouse virulence of two K antigen-containing (L variety) strains of Escherichia coli (serotype O2:K1) isolated from human septicemia, and of their variants which lacked K antigen, was studied. The strains containing envelope antigen (K+) were highly virulent when injected intracerebrally or when suspended in mucin and injected intraperitoneally. After intraperitoneal injection of E-107 K+ (but not K−), there was a marked initial growth in the peritoneal cavity followed by bacteremia and infection of all the organs examined. In the mucin-enhanced lethal infection, this growth continued until death of the animal; in the nonlethal infection, growth ceased and the count dropped quickly after approximately 5 hr. Host defenses were depressed greatly by intraperitoneally, but not intravenously, administered mucin. Bacteria were most virulent when injected intraperitoneally. In vitro phagocytosis of the K+ bacteria required opsonins not needed for phagocytosis of the smooth K− variants. Opsonins were found in immunized rabbit and normal mouse sera. Immune rabbit sera contained antibodies with anti-K specificity which were opsonic in vitro and highly protective in vivo when administered passively. There appears to be a lesser anti-O opsonic and protective activity involving one of the strains (E-107 K+), and colonial morphology, agglutination, and absorption tests indicated a low amount of K antigen on this organism. No anti-O opsonic or protective activity could be shown involving the other strain (E-102 K+). When standard serological typing procedures were used, these two strains appeared to be identical serologically, but they differed greatly in sensitivity to immune rabbit serum in phagocytosis experiments in vitro.     

Affinity regulates spatial range of EGF receptor autocrine ligand binding

Proper spatial localization of EGFR signaling activated by autocrine ligands represents a critical factor in embryonic development as well as tissue organization and function, and ligand/receptor binding affinity is among the molecular and cellular properties suggested to play a role in governing this localization. We employ a computational model to predict how receptor-binding affinity affects local capture of autocrine ligand vis-a-vis escape to distal regions, and provide experimental test by constructing cell lines expressing EGFR along with either wild-type EGF or a low-affinity mutant, EGF(L47M). The model predicts local capture of a lower affinity autocrine ligand to be less efficient when the ligand production rate is small relative to receptor appearance rate. Our experimental data confirm this prediction, demonstrating that cells can use ligand/receptor binding affinity to regulate ligand spatial distribution when autocrine ligand production is limiting for receptor signaling.