Return Customers: Foraging Site Fidelity and the Effect of Environmental Variability in Wide-Ranging Antarctic Fur Seals

Strategies employed by wide-ranging foraging animals involve consideration of habitat quality and predictability and should maximise net energy gain. Fidelity to foraging sites is common in areas of high resource availability or where predictable changes in resource availability occur. However, if resource availability is heterogeneous or unpredictable, as it often is in marine environments, then habitat familiarity may also present ecological benefits to individuals. We examined the winter foraging distribution of female Antarctic fur seals, Arctocephalus gazelle, over four years to assess the degree of foraging site fidelity at two scales; within and between years. On average, between-year fidelity was strong, with most individuals utilising more than half of their annual foraging home range over multiple years. However, fidelity was a bimodal strategy among individuals, with five out of eight animals recording between-year overlap values of greater than 50%, while three animals recorded values of less than 5%. High long-term variance in sea surface temperature, a potential proxy for elevated long-term productivity and prey availability, typified areas of overlap. Within-year foraging site fidelity was weak, indicating that successive trips over the winter target different geographic areas. We suggest that over a season, changes in prey availability are predictable enough for individuals to shift foraging area in response, with limited associated energetic costs. Conversely, over multiple years, the availability of prey resources is less spatially and temporally predictable, increasing the potential costs of shifting foraging area and favouring long-term site fidelity. In a dynamic and patchy environment, multi-year foraging site fidelity may confer a long-term energetic advantage to the individual. Such behaviours that operate at the individual level have evolutionary and ecological implications and are potential drivers of niche specialization and modifiers of intra-specific competition.     

Aleutian Mink Disease Virus in Free-Ranging Mink from Sweden

Aleutian mink disease (AMD) is a chronic viral disease in farmed mink and the virus (AMDV) has been found in many free-ranging mink (Neovison vison) populations in Europe and North America. In this study, AMDV DNA and AMDV antibodies were analysed in 144 free-ranging mink hunted in Sweden. Associations between being AMDV infected (defined as positive for both viral DNA and antibodies) and the weight of the spleen, liver, kidneys, adrenal glands and body condition were calculated and the sequences of ten AMDV isolates were analysed in order to characterize the genetic relationships. In total, 46.1% of the mink were positive for AMDV antibodies and 57.6% were positive for AMDV DNA. Twenty-two percent of the mink tested on both tests (n = 133) had dissimilar results. The risk of having AMDV antibodies or being positive for AMDV DNA clearly increased with age and the majority of the mink that were two years or older were infected. Few macroscopic changes were found upon necropsy. However, the relative weight of the spleen was sexually dimorphic and was found to be slightly, but significantly (p = 0.006), heavier in AMDV infected male mink than uninfected. No association between AMDV infection and body condition, weight of the kidneys, liver or adrenal glands were found. Several different strains of AMDV were found across the country. Two of the AMDV sequences from the very north of Sweden did not group with any of the previously described groups of strains. In summary, AMDV seems to be prevalent in wild mink in Sweden and may subtly influence the weight of the spleen.     

Prevalence of allosuckling behaviour in Subantarctic fur seal pups

Non-offspring maternal care should be rare due to the high costs of raising offspring, particularly lactation, but nonetheless occurs in a variety of taxa. Misguided parental care, associated with recognition errors and/or inattentiveness by lactating females, has been hypothesized as an explanation for allolactation in mammals. In an extension of this hypothesis, we suggest that milk-stealing is parasitism instigated by non-filial offspring, and that maternal behaviour is of secondary interest in an evolutionary context if she is unaware of the interaction. We provide evidence for frequent milk-stealing attempts by Subantarctic fur seal (Arctocephalus tropicalis) pups, including an example of sustained non-maternal care (> three months) for one pup during the confirmed absence of his mother, leading to a weaning mass equal to the population mean. We also present only the second account of fostering/twins in the species at this locality. We suggest that rather than the hitherto suggested rare and anomalous behaviour, milk-stealing behaviour (while not always successful) is common.     

Comparison of the PKCalpha and the PKCepsilon C1b domains: identification of residues critical for PKCepsilon-mediated neurite induction

We showed earlier that over-expression of protein kinase C (PKC) epsilon induces neurite outgrowth. The effect is mediated by a region (PKCepsilonPSC1V3) encompassing the pseudosubstrate, the two C1 domains and part of the V3 region, and is independent of the catalytic activity of the enzyme. In this region, residues immediately N-terminal of the C1b domain are crucial for neurite outgrowth. However, in this study we show that the PKCepsilon C1b domain itself is necessary for neurite induction, since a mutant in which the PKCepsilon C1b domain has been replaced with the C1b domain from PKCalpha, PKCepsilonPSC1a(alphaC1b)V3 lacks neurite-inducing capacity. The molecular basis for the importance of the PKCepsilon C1b domain was investigated by mutation studies of the PKCalpha C1b domain. Point mutations were done in the PKCalpha C1b domain of the PKCepsilonPSC1a(alphaC1b)V3 construct, in which the PKCalpha residues were mutated into the corresponding residues in PKCepsilon. This highlighted residues in the C-terminal part of the primary sequence of the C1b domain, located in the base of the C1b domain, as important for neurite outgrowth. The mutations S48P, D32K and L49N all influenced neurite induction positively. Furthermore, the mutation of L49N alone was sufficient to make PKCepsilonPSC1a(alphaC1b)V3 neuritogenic in phorbol ester-stimulated cells, and mutation of this residue in full-length PKCepsilon into the corresponding residue in PKCalpha, N291L reduced the neurite-inducing effect of PKCepsilon. In conclusion, we have identified residues in the PKCepsilon C1b domain, in particular Asn49, that are essential for neurite outgrowth.     

Liver cell death and anemia in Wilson disease involve acid sphingomyelinase and ceramide

Wilson disease is caused by accumulation of Cu(2+) in cells, which results in liver cirrhosis and, occasionally, anemia. Here, we show that Cu(2+) triggers hepatocyte apoptosis through activation of acid sphingomyelinase (Asm) and release of ceramide. Genetic deficiency or pharmacological inhibition of Asm prevented Cu(2+)-induced hepatocyte apoptosis and protected rats, genetically prone to develop Wilson disease, from acute hepatocyte death, liver failure and early death. Cu(2+) induced the secretion of activated Asm from leukocytes, leading to ceramide release in and phosphatidylserine exposure on erythrocytes, events also prevented by inhibition of Asm. Phosphatidylserine exposure resulted in immediate clearance of affected erythrocytes from the blood in mice. Accordingly, individuals with Wilson disease showed elevated plasma levels of Asm, and displayed a constitutive increase of ceramide- and phosphatidylserine-positive erythrocytes. Our data suggest a previously unidentified mechanism for liver cirrhosis and anemia in Wilson disease.     

Enrichment of electrochemically active bacteria using a three-electrode electrochemical cell

Electrochemically active bacteria were successfully enriched in an electrochemical cell using a positively poised working electrode. The positively poised working electrode (+0.7 V vs. Ag/AgCl) was used as an electron acceptor for enrichment and growth of electrochemically active bacteria. When activated sludge and synthetic wastewater were fed to the electrochemical cell, a gradual increase in amperometric current was observed. After a period of time in which the amperometric current was stabilized (generally 8 days), linear correlations between the amperometric signals from the electrochemical cell and added BOD (biochemical oxygen demand) concentrations were established. Cyclic voltammetry of the enriched electrode also showed prominent electrochemical activity. When the enriched electrodes were examined with electron microscopy and confocal scanning laser microscopy, a biofilm on the enriched electrode surface and bacterium-like particles were observed. These experimental results indicate that the electrochemical system in this study is a useful tool for the enrichment of an electrochemically active bacterial consortium and could be used as a novel microbial biosensor.     

Empirical comparison of tests for differential expression on time-series microarray experiments

Methods for identifying differentially expressed genes were compared on time-series microarray data simulated from artificial gene networks. Select methods were further analyzed on existing immune response data of Boldrick et al. (2002, Proc. Natl. Acad. Sci. USA 99, 972-977). Based on the simulations, we recommend the ANOVA variants of Cui and Churchill. Efron and Tibshirani's empirical Bayes Wilcoxon rank sum test is recommended when the background cannot be effectively corrected. Our proposed GSVD-based differential expression method was shown to detect subtle changes. ANOVA combined with GSVD was consistent on background-normalized simulation data. GSVD with empirical Bayes was consistent without background correction. Based on the Boldrick et al. data, ANOVA is best suited to detect changes in temporal data, while GSVD and empirical Bayes effectively detect individual spikes or overall shifts, respectively. For methods tested on simulation data, lowess after background correction improved results. On simulation data without background correction, lowess decreased performance compared to median centering.     

Loss of hepatic chaperone‐mediated autophagy accelerates proteostasis failure in aging

Chaperone‐mediated autophagy (CMA), a cellular process that contributes to protein quality control through targeting of a subset of cytosolic proteins to lysosomes for degradation, undergoes a functional decline with age. We have used a mouse model with liver‐specific defective CMA to identify changes in proteostasis attributable to reduced CMA activity in this organ with age. We have found that other proteolytic systems compensate for CMA loss in young mice which helps to preserve proteostasis. However, these compensatory responses are not sufficient for protection against proteotoxicity induced by stress (oxidative stress, lipid challenges) or associated with aging. Livers from old mice with CMA blockage exhibit altered protein homeostasis, enhanced susceptibility to oxidative stress and hepatic dysfunction manifested by a diminished ability to metabolize drugs, and a worsening of the metabolic dysregulation identified in young mice. Our study reveals that while the regulatory function of CMA cannot be compensated for in young organisms, its contribution to protein homeostasis can be handled by other proteolytic systems. However, the decline in the compensatory ability identified with age explains the more severe consequences of CMA impairment in older organisms and the contribution of CMA malfunction to the gradual decline in proteostasis and stress resistance observed during aging.