Circannual variation in habitat use of the White-winged Snowfinch Montifringilla nivalis nivalis

High mountain areas are subject to strong seasonal fluctuations, and species inhabiting these particular environments show a high degree of habitat specialization to cope with extreme abiotic conditions. Estimates of habitat use are influenced by the spatial and seasonal scales at which they are evaluated, so studies at multiple scales are important in order to explore adaptive responses to seasonal environments. In the present study, we assessed habitat use of the White-winged Snowfinch Montifringilla nivalis subsp. nivalis (henceforth Snowfinch) during breeding and non-breeding seasons at three different spatial scales (diameters of 100, 250 and 500 m). Although Snowfinches clearly used high-elevation habitats in both seasons, there was evidence that they are less specific during the non-breeding period: the variance explained by habitat and topographical factors was lower in winter than in the breeding season. Moreover, our results suggest that the use of habitat is scale-dependent. This pattern was especially relevant in the breeding season, perhaps because habitat use might be more related to nest-site selection and specific foraging sites to provide food for nestlings. Snowfinches use high mountain habitats throughout the year, probably as a consequence of physiological and morphological specializations typical of high-elevation species, but in winter they show a certain flexibility in habitat use. Snowfinches might thus adopt a flexible specialist strategy. This could represent a trade-off to overcome possible effects on survival, condition and fitness, which can be particularly strong in harsh, unpredictable environments.     

Inertia: the discrepancy between individual and common good in dispersal and prospecting behaviour

The group selection debate of the 1960s made it clear that evolution does not necessarily increase population performance. Individuals can be selected to have traits that diminish a common good and make population persistence difficult. At the extreme, the discrepancy between levels of selection is predicted to make traits evolve towards values at which a population can no longer persist (evolutionary suicide). Dispersal and prospecting are prime examples of traits that have a strong influence on population persistence under environmental and demographic stochasticity. Theory predicts that an ‘optimal’ dispersal strategy from a population point of view can differ considerably from that produced by individual‐level selection. Because dispersal is frequently risky or otherwise costly, individuals are often predicted to disperse less than would be ideal for population performance (persistence or size). We define this discrepancy as ‘inertia’ and examine current knowledge of its occurrence and effects on population dynamics in nature. We argue that inertia is potentially widespread but that a framework is currently lacking for predicting precisely the extent to which it has a real influence on population persistence. The opposite of inertia, ‘hypermobility’ (more dispersal by individuals than would maximize population performance) remains a possibility: it is known that highest dispersal rates do not lead to best expected population performance, and examples of such high dispersal evolving exist at least in the theoretical literature. We also show, by considering prospecting behaviour, that similar issues arise in species with advanced cognitive and learning abilities. Individual prospecting strategies and the information acquired during dispersal are known to influence the decisions and therefore the fate of individuals and, as a corollary, populations. Again, the willingness of individuals to sample environments might evolve to levels that are not optimal for populations. This conflict can take intriguing forms. For example, better cognitive abilities of individuals may not always lead to better population‐level performance. Simulation studies have found that ‘blind’ dispersal can lead to better connected metapopulations than cognitively more advanced habitat choice rules: the latter can lead to too many individuals sticking to nearby safe habitat. The study of the mismatch between individual and population fitness should not be a mere intellectual exercise. Population managers typically need to take a population‐level view of performance, which may necessitate human intervention if it differs from what is selected for. We conclude that our knowledge of inertia and hypermobility would advance faster if theoretical studies—without much additional effort—quantified the population consequences of the evolving traits and compared this with hypothetical (not selectively favoured) dispersal rules, and if empirical studies were similarly conducted with the differing levels of selection in mind.     

An evolutionary trade-off between protein turnover rate and protein aggregation favors a higher aggregation propensity in fast degrading proteins

We previously showed the existence of selective pressure against protein aggregation by the enrichment of aggregation-opposing 'gatekeeper' residues at strategic places along the sequence of proteins. Here we analyzed the relationship between protein lifetime and protein aggregation by combining experimentally determined turnover rates, expression data, structural data and chaperone interaction data on a set of more than 500 proteins. We find that selective pressure on protein sequences against aggregation is not homogeneous but that short-living proteins on average have a higher aggregation propensity and fewer chaperone interactions than long-living proteins. We also find that short-living proteins are more often associated to deposition diseases. These findings suggest that the efficient degradation of high-turnover proteins is sufficient to preclude aggregation, but also that factors that inhibit proteasomal activity, such as physiological ageing, will primarily affect the aggregation of short-living proteins.     

Feeding time synchronizes clock gene rhythmic expression in brain and liver of goldfish (Carassius auratus)

Little is known about the feeding time dependence of clock gene expression in fish. The aim of the present study was to investigate whether a scheduled feeding time can entrain the rhythmic expression of several clock genes (period and cryptocrome) in the brain and liver of a teleost, the goldfish. Fish maintained under continuous light (LL) conditions were divided into 3 groups. Two groups were fed daily at 1000 h and 2200 h, respectively, and the third group was subjected to a random schedule regime. After 30 days, the fishes under 24-h food deprivation were sacrificed through a 24-h cycle, and clock gene expression in the optic tectum, hypothalamus, and liver was quantified by real-time PCR. The findings pointed to differences between the central and peripheral tissues studied. In the absence of a light-dark cycle (constant light), a scheduled feeding regime was necessary and sufficient to maintain both the rhythmic expression of several clock genes in the optic tectum and hypothalamus, as well as daily rhythms in locomotor activity. In contrast, neither locomotor activity nor clock gene expression in brain tissues was synchronized in randomly fed fish. However, in the liver, most of the clock genes studied presented significant daily rhythms in phase (related to the time of the last meal) in all 3 experimental groups, suggesting that the daily rhythm of clock genes in this organ only depends on the last meal time. The data suggest that, as in mammals, the smooth running of the food entrainable oscillator (FEO) in fish involves the rhythmic expression of several clock genes (Per1 and Cry3) in the central and peripheral structures. The results also indicate that the food anticipatory activity (FAA) in goldfish is not only the result of rhythmic clock gene expression in the liver because rhythmic clock gene expression was observed in randomly fed fishes, while FAA was not observed.     

Isolation of a novel Aggregatibacter actinomycetemcomitans serotype b bacteriophage capable of lysing bacteria within a biofilm

A bacteriophage specific for Aggregatibacter actinomycetemcomitans serotype b, able to kill the bacterium within a biofilm, was isolated. Random mutagenesis of this phage rendered a bacteriophage able to kill 99% of the bacteria within a biofilm. This is the first report of a biocontrol experiment against A. actinomycetemcomitans.     

Density-functional study on the equilibria in the ThDP activation

The equilibria among the various ionization and tautomeric states involved in the activation of ThDP is addressed using high level density functional theory calculations, X3LYP/6-311++G(d,p)//X3LYP(PB)/6-31++G(d,p). This study provides the first theoretically derived thermodynamic data for the internal equilibria in the activation of ThDP. The role of the medium polarity on the geometry and thermodynamics of the diverse equilibria of ThDP is addressed. The media chosen are cyclohexane and water, as paradigms of apolar and polar media. The results suggest that all ionization and tautomeric states are accessible during the catalytic cycle, even in the absence of substrate, being APH⁺ the form required to interconvert the AP and IP tautomers; and the generation of the ylide proceeds via the formation of the IP form. Additionally, the calculated ΔG° values allow to calculate all the equilibrium constants, including the pK_C2 for the thiazolium C2 atom whose ionization is believed to initiate the catalytic cycle.     

RyRCa2+ leak limits cardiac Ca2+ window current overcoming the tonic effect of calmodulinin mice

Ca(2+) mediates the functional coupling between L-type Ca(2+) channel (LTCC) and sarcoplasmic reticulum (SR) Ca(2+) release channel (ryanodine receptor, RyR), participating in key pathophysiological processes. This crosstalk manifests as the orthograde Ca(2+)-induced Ca(2+)-release (CICR) mechanism triggered by Ca(2+) influx, but also as the retrograde Ca(2+)-dependent inactivation (CDI) of LTCC, which depends on both Ca(2+) permeating through the LTCC itself and on SR Ca(2+) release through the RyR. This latter effect has been suggested to rely on local rather than global Ca(2+) signaling, which might parallel the nanodomain control of CDI carried out through calmodulin (CaM). Analyzing the CICR in catecholaminergic polymorphic ventricular tachycardia (CPVT) mice as a model of RyR-generated Ca(2+) leak, we evidence here that increased occurrence of the discrete local SR Ca(2+) releases through the RyRs (Ca(2+) sparks) cause a depolarizing shift in activation and a hyperpolarizing shift in isochronic inactivation of cardiac LTCC current resulting in the reduction of window current. Both increasing fast [Ca(2+)](i) buffer capacity or depleting SR Ca(2+) store blunted these changes, which could be reproduced in WT cells by RyRCa(2+) leak induced with Ryanodol and CaM inhibition.Our results unveiled a new paradigm for CaM-dependent effect on LTCC gating and further the nanodomain Ca(2+) control of LTCC, emphasizing the importance of spatio-temporal relationships between Ca(2+) signals and CaM function.