Actin is a component of the compensation mechanism in pseudorabies virus virions lacking the major tegument protein VP22

Despite being a major component of the pseudorabies virus tegument, VP22 is not required for PRV replication, virulence, or neuroinvasion (T. del Rio, H. C. Werner, and L. W. Enquist, J. Virol. 76:774-782, 2002). In the absence of VP22, tegument assembly compensates in a limited fashion with increased incorporation of cellular actin. Infection of epithelial cell lines expressing fluorescent actin fusion proteins resulted in the incorporation of filamentous and nonfilamentous actin into individual virions that were predominately light, noninfectious particles. We conclude that cellular actin is incorporated in the tegument of wild-type virions and is part of a compensation mechanism for VP22-null virions.     

Herpes simplex virus type 1 glycoprotein e is required for axonal localization of capsid, tegument, and membrane glycoproteins

Herpes simplex virus type 1 (HSV-1) glycoprotein E (gE) promotes cell-to-cell spread at basolateral surfaces of epithelial cells, but its activity in neurons is less clear. We used the mouse retina infection model and neuronal cell cultures to define the spread phenotype of gE mutant viruses. Wild-type (WT) and gE-null (NS-gEnull) viruses both infected retina ganglion cell neurons; however, NS-gEnull viral antigens failed to reach the optic nerve, which indicates a defect in axonal localization. We evaluated two Fc receptor-negative gE mutant viruses containing four amino acid inserts in the gE ectodomain. One mutant virus failed to spread from the retina into the optic nerve, while the other spread normally. Therefore, the gE ectodomain is involved in axonal localization, and the Fc receptor and neuronal spread are mediated by overlapping but distinct gE domains. In the retina infection model, virus can travel to the brain via the optic nerve from presynaptic to postsynaptic neurons (anterograde direction) or via nerves that innervate the iris and ciliary body from postsynaptic to presynaptic neurons (retrograde direction). WT virus infected the brain by anterograde and retrograde routes, whereas NS-gEnull virus failed to travel by either pathway. The site of the defect in retrograde spread remains to be determined; however, infection of rat superior cervical ganglia neurons in vitro indicates that gE is required to target virion components to the axon initial segment. The requirement for gE in axonal targeting and retrograde spread highlights intriguing similarities and differences between HSV-1 and pseudorabies virus gE.     

Heterogeneity of a fluorescent tegument component in single pseudorabies virus virions and enveloped axonal assemblies

The molecular mechanisms responsible for long-distance, directional spread of alphaherpesvirus infections via axons of infected neurons are poorly understood. We describe the use of red and green fluorescent protein (GFP) fusions to capsid and tegument components, respectively, to visualize purified, single extracellular virions and axonal assemblies after pseudorabies virus (PRV) infection of cultured neurons. We observed heterogeneity in GFP fluorescence when GFP was fused to the tegument component VP22 in both single extracellular virions and discrete puncta in infected axons. This heterogeneity was observed in the presence or absence of a capsid structure detected by a fusion of monomeric red fluorescent protein to VP26. The similarity of the heterogeneous distribution of these fluorescent protein fusions in both purified virions and in axons suggested that tegument-capsid assembly and axonal targeting of viral components are linked. One possibility was that the assembly of extracellular and axonal particles containing the dually fluorescent fusion proteins occurred by the same process in the cell body. We tested this hypothesis by treating infected cultured neurons with brefeldin A, a potent inhibitor of herpesvirus maturation and secretion. Brefeldin A treatment disrupted the neuronal secretory pathway, affected fluorescent capsid and tegument transport in the cell body, and blocked subsequent entry into axons of capsid and tegument proteins. Electron microscopy demonstrated that in the absence of brefeldin A treatment, enveloped capsids entered axons, but in the presence of the inhibitor, unenveloped capsids accumulated in the cell body. These results support an assembly process in which PRV capsids acquire a membrane in the cell body prior to axonal entry and subsequent transport.     

Spots and stripes: the evolution of repetition in visual signal form

It is common to find spatially repetitive patterns in animal visual signals. The evolution of such patterns is not well explained by existing theories of signal evolution. In this paper, we suggest that the evolution of signals with spatial repetition may be due to specific recognition problems and receiver biases. The logics of our hypotheses are studied in co-evolutionary simulations using artificial neural networks as models of receivers. These simulations yield repetitive visual signals under the following conditions: translations and reflections of the signal, partial obstruction of the signal, a fixed feature in the signal, and lateral inhibition in the receiver. In addition to regular repetitions our simulations sometimes result in other organisations of the signal such as blocky patterns and gradients.     

The effects of selection,drift and genetic variation on life‐history trait divergence among insular populations of natterjack toad,Bufo calamita

Although loss of genetic variation is frequently assumed to be associated with loss of adaptive potential, only few studies have examined adaptation in populations with little genetic variation. On the Swedish west coast, the northern fringe populations of the natterjack toad Bufo calamita inhabit an atypical habitat consisting of offshore rock islands. There are strong among‐population differences in the amount of neutral genetic variation, making this system suitable for studies on mechanisms of trait divergence along a gradient of within‐population genetic variation. In this study, we examined the mechanisms of population divergence using Q_ST–F_ST comparisons and correlations between quantitative and neutral genetic variation. Our results suggest drift or weak stabilizing selection across the six populations included in this study, as indicated by low Q_ST–F_ST values, lack of significant population × temperature interactions and lack of significant differences among the islands in breeding pond size. The six populations included in this study differed in both neutral and quantitative genetic variation. Also, the correlations between neutral and quantitative genetic variation tended to be positive, however, the relatively small number of populations prevents any strong conclusions based on these correlations. Contrary to the majority of Q_ST–F_ST comparisons, our results suggest drift or weak stabilizing selection across the examined populations. Furthermore, the low heritability of fitness‐related traits may limit evolutionary responses in some of the populations.     

Functional integration of adult-born neurons

Over the past decade, it has become clear that neural stem cells in the adult mammalian brain continuously generate new neurons, predominantly in the hippocampus and olfactory bulb. However, the central issue of whether these new neurons participate in functional synaptic circuitry has yet to be resolved. Here, we use virus-based transsynaptic neuronal tracing and c-Fos mapping of odor-induced neuronal activity to demonstrate that neurons generated in the adult functionally integrate into the synaptic circuitry of the brain.     

Polar bear (Ursus maritimus) cub mortality at a den site in northern Alaska

In March 2009, we documented the death of one member of a triplet polar bear (Ursus maritimus) litter at its den site in the southern Beaufort Sea (SBS) of Alaska. We used a self-contained video camera unit to document activity between den emergence and departure. All three cubs showed low activity levels relative to other cubs observed, and one died within one week of den emergence. Necropsy confirmed that the dead cub had a low body weight and was malnourished. Capture later confirmed that the two surviving cubs were also undersized. Polar bear cub survival is influenced by many factors including litter size and sea ice conditions. Triplet litters are often smaller and suffer higher mortality rates than singletons and twins. This cub was not only a triplet but also born following 2 years of record minimum sea ice extent, both of which may have played a role in this cub’s demise.     

The return of the variance: intraspecific variability in community ecology

Despite being recognized as a promoter of diversity and a condition for local coexistence decades ago, the importance of intraspecific variance has been neglected over time in community ecology. Recently, there has been a new emphasis on intraspecific variability. Indeed, recent developments in trait-based community ecology have underlined the need to integrate variation at both the intraspecific as well as interspecific level. We introduce new T-statistics ('T' for trait), based on the comparison of intraspecific and interspecific variances of functional traits across organizational levels, to operationally incorporate intraspecific variability into community ecology theory. We show that a focus on the distribution of traits at local and regional scales combined with original analytical tools can provide unique insights into the primary forces structuring communities.     

Evolving ecological networks and the emergence of biodiversity patterns across temperature gradients

In ectothermic organisms, it is hypothesized that metabolic rates mediate influences of temperature on the ecological and evolutionary processes governing biodiversity. However, it is unclear how and to what extent the influence of temperature on metabolism scales up to shape large-scale diversity patterns. In order to clarify the roles of temperature and metabolism, new theory is needed. Here, we establish such theory and model eco-evolutionary dynamics of trophic networks along a broad temperature gradient. In the model temperature can influence, via metabolism, resource supply, consumers' vital rates and mutation rate. Mutation causes heritable variation in consumer body size, which diversifies and governs consumer function in the ecological network. The model predicts diversity to increase with temperature if resource supply is temperature-dependent, whereas temperature-dependent consumer vital rates cause diversity to decrease with increasing temperature. When combining both thermal dependencies, a unimodal temperature-diversity pattern evolves, which is reinforced by temperature-dependent mutation rate. Studying coexistence criteria for two consumers showed that these outcomes are owing to temperature effects on mutual invasibility and facilitation. Our theory shows how and why metabolism can influence diversity, generates predictions useful for understanding biodiversity gradients and represents an extendable framework that could include factors such as colonization history and niche conservatism.