Nicotine enhances intracellular nicotinic receptor maturation: a novel mechanism of neural plasticity?

Nicotine addiction, the primary cause of tobacco consumption, is mediated through nicotine binding to brain nicotinic acetylcholine receptor (nAChRs). Upon chronic exposure, nicotine elicits a cascade of events, starting with nAChR activation and desensitization, followed by a long term up-regulation that corresponds to an increase in the number of the high affinity nAChRs, a paradoxical process that occurs in the brain of smokers. Recent investigation of the maturation and trafficking of the major brain alpha4beta2 nAChR demonstrates that up-regulation is initiated in the endoplasmic reticulum soon after protein translation. The data thus far accumulated provide evidence that nicotine elicits up-regulation by promoting maturation of nAChR precursors that would otherwise be degraded. This "maturational enhancer" action of nicotine probably contributes to the long term effect of chronic nicotine, and suggests a novel mechanism of neuronal plasticity through an yet unknown endogenous substance which would modulate the receptor expression under physiological conditions.     

Responses of disparate phenotypically-plastic,melanin-based traits to common cues: limits to the benefits of adaptive plasticity?

The evolution of perfect adaptive phenotypic plasticity of a given trait may be influenced by, among other things, phenotypic costs associated with the expression of a given trait value, relative to alternative trait values. One potential cause of such phenotypic costs is the allocation of limited resources to multiple traits. When multiple traits rely on the same resource, trait values for one adaptively plastic trait might be unavoidably associated with maladaptive trait values for other traits. I address this problem in three traits of Pieris rapae L. (the small cabbage white butterfly) that all rely on the pigment melanin and are adaptively plastic, but have very different functions: wing pattern, immune defense, and pupal color. Cool, short-day rearing conditions simultaneously increased total wing melanization and decreased a melanin-based immune response in females, consistent with predictions. However, cool, short days also reduced the melanin-based immune response in males, despite little effect on male wing melanization. Furthermore, contrary to predictions, these patterns were not altered by differences in dietary resources. Finally, dark-colored rearing backgrounds during pupation substantially increased pupal melanization in both sexes, but was not associated with differences in wing melanization. These results offer only mixed support for the hypothesis of melanin-based trade offs as a source of phenotypic costs to adaptive plasticity in these traits. However, patterns of sexual dimorphism for these traits suggest trade offs might be at work at another level: relative to males, females have consistently more heavily melanized wings but less heavily melanized pupae and immune responses. The reduced immune response under cool, short-day conditions may also have implications for the evolutionary ecology of these butterflies.     

Activation segment exchange: a common mechanism of kinase autophosphorylation?

The crystal structure of the kinase domain from human checkpoint kinase 2 (Chk2) has shown, for the first time, the reciprocal exchange of activation segments between two adjacent molecules and provides the molecular basis for understanding the observed mode of Chk2 kinase activation via trans-autophosphorylation. With further examples of activation segment exchanged kinase domains now publicly available (i.e. Ste20-like kinase, Ser/Thr kinase 10 and Death-associated protein kinase 3), we suggest that this phenomenon represents a common mechanism of activation amongst a particular subset of protein kinases, that is, those that are dimeric (either transiently or constitutively), that undergo activation by autophosphorylation and that have activation segment amino acid sequences that do not resemble those of their substrate consensus sequence.     

Degradation of negative regulators: a common theme in hormone and light signaling networks?

Signal transduction pathways often modulate both positively and negatively acting components to optimize the efficiency of a signal. Recent results have shown that plants make extensive use of regulated proteolysis to modulate signal transduction pathways. An emerging theme from hormone (e.g. auxin and gibberellin) and light signaling pathways is signal or stimulus-induced degradation of negative regulators to optimize plant growth and development.     

Maternal steroids and contaminants in common tern eggs: a mechanism of endocrine disruption?

We looked for evidence for the hypothesis that exposure of female birds to polychlorinated biphenyls (PCBs) results in alteration of blood steroid hormone concentrations and alters subsequent hormone transfer of steroids to eggs. Eggs of three-egg clutches were collected from a PCB-exposed common tern (Sterna hirundo) colony (Ram Island, Buzzards Bay, MA, USA) and from a relatively clean colony (Bodkin Island, Chesapeake Bay, MD, USA), and were analyzed for concentrations of organochlorine contaminants and steroid hormones (17beta-estradiol, 5alpha-dihydrotestosterone, testosterone and androstenedione). There was no relationship between total PCBs and steroid concentrations considering all eggs together, considering eggs of different laying order or considering differences between sequentially laid eggs in a clutch. Similarly, concentrations of di- and tri-chlorinated biphenyls and steroids in eggs were not related. The concentrations of PCBs, mercury and selenium were below estimated thresholds for toxicity to embryos. Maternal steroids, except estradiol, were present in yolk of all eggs, with increasing concentrations in the second and third eggs laid. Our data provided no evidence for a maternal toxicological event that might alter the amount of maternal steroid hormone transferred to eggs.     

Surface transport properties of reticulopodia: do intracellular and extracellular motility share a common mechanism?

The reticulopodial networks of the foraminiferan protozoans Allogromia sp., strain NF, and A. laticollaris display rapid (up to 11 microns/second) and bidirectional saltatory transport of membrane surface markers (polystyrene microspheres). Electron microscopy shows that microspheres adhere directly to the reticulopodial surface glycocalyx. A videomicroscopic analysis of this phenomenon reveals that microsphere movement is typically independent of pseudopod extension/withdrawal and that particles of different sizes and surface properties display similar motile characteristics. The motile properties of surface-associated microspheres appear identical to those of saltating intracellular organelles. Indeed, in some instances the surface-attached microspheres appear transiently linked in motion to these underlying organelles. Our observations suggest that, in reticulopodia, surface transport of microspheres and intracellular transport of organelles are driven by a common mechanism.     

Shading and texture: separate information channels with a common adaptation mechanism?

We outline a scheme for the way in which early vision may handle information about shading (luminance modulation, LM) and texture (contrast modulation, CM). Previous work on the detection of gratings has found no sub-threshold summation, and no cross-adaptation, between LM and CM patterns. This strongly implied separate channels for the detection of LM and CM structure. However, we now report experiments in which adapting to LM (or CM) gratings creates tilt aftereffects of similar magnitude on both LM and CM test gratings, and reduces the perceived strength (modulation depth) of LM and CM gratings to a similar extent. This transfer of aftereffects between LM and CM might suggest a second stage of processing at which LM and CM information is integrated. The nature of this integration, however, is unclear and several simple predictions are not fulfilled. Firstly, one might expect the integration stage to lose identity information about whether the pattern was LM or CM. We show instead that the identity of barely detectable LM and CM patterns is not lost. Secondly, when LM and CM gratings are combined in-phase or out-of-phase we find no evidence for cancellation, nor for 'phase-blindness'. These results suggest that information about LM and CM is not pooled or merged--shading is not confused with texture variation. We suggest that LM and CM signals are carried by separate channels, but they share a common adaptation mechanism that accounts for the almost complete transfer of perceptual aftereffects.     

Somatic plasticity of neural stem cells: Fact or fancy?

Several studies have described the potential for embryonic and adult neural stem cells to differentiate into non-neural cells such as muscle and blood, tissues that are derived from non-neuroectodermal germ layers. This raised the exciting possibility that these cells possessed a broader range of differentiation potential than originally thought and raised interesting prospects for possible transplantation utilization. However, a number of recent reports have raised questions about whether the phenomena observed actually represented true somatic plasticity. In this review, we critically analyze these studies with the aim of providing some criteria by which future studies that address this important problem may be evaluated.     

Small heat-shock proteins and clusterin: intra- and extracellular molecular chaperones with a common mechanism of action and function?

Small heat-shock proteins (sHsps) and clusterin are molecular chaperones that share many functional similarities despite their lack of significant sequence similarity. These functional similarities, and some differences, are discussed. sHsps are ubiquitous intracellular proteins whereas clusterin is generally found extracellularly. Both chaperones potently prevent the amorphous aggregation and precipitation of target proteins under stress conditions such as elevated temperature, reduction and oxidation. In doing so, they act on the slow, off-folding protein pathway. The conformational dynamism and aggregated state of both proteins may be crucial for their chaperone function. Subunit exchange is likely to be important in regulating chaperone action; the dissociated form of the protein is probably the chaperone-active species rather than the aggregated state. They both exert their chaperone action without the need for hydrolysis of ATP and have little ability to refold target proteins. Increased expression of sHsps and clusterin accompanies a range of diseases that arise from protein misfolding and deposition of highly structured protein aggregates known as amyloid fibrils, e.g., Alzheimer's, Creutzfeldt-Jakob and Parkinson's diseases. The interaction of sHsps and clusterin with fibril-forming species is discussed along with their ability to prevent fibril formation.     

Induction of preference and performance after acclimation to novel hosts in a phytophagous spider mite: adaptive plasticity?

We examined induction of preference and performance on novel host plants for two laboratory populations of the polyphagous spider mite Tetranychus urticae, with one population adapted to bean and the other population adapted to tomato. We bred four isofemale lines of the bean population only and used them in all the assays. The bean population had a 30% lower fecundity on tomato than on bean, while the tomato population had equal fecundity on both host plants. Acclimation of adult females to the novel host plant for both populations increased acceptability of that novel host but did not increase rejection of the original host. The bean population experienced a 60% benefit and a 30% cost in terms of egg production for acclimating to tomato, thus exemplifying adaptive plasticity. The tomato population showed a 23% benefit for acclimating to bean but no cost. Mites from the bean population that were acclimated to tomato fed more on tomato than did mites that were not acclimated to tomato. When these mites were fed inhibitors of cytochrome P-450 detoxification enzymes, their performance was severely depressed (84%) on tomato but not on bean. However, mites that were fed inhibitors of P-450 enzymes did not reduce their acceptance of tomato as a host. Thus, performance on novel hosts (but not preference) in this species is likely correlated with the induction of detoxifying enzymes. Spider mites are known to form host races rapidly on novel hosts. Induction of preference and physiological acclimation via detoxification enzymes may enhance performance and, thus, strongly contribute to initial stages of host race formation.     

Phylloxera and the grapevine: a sense of common purpose?

The purpose of life is its continuation: survival is the reason things live. Here we explore this 'basic' of biology, by reference to the extraordinary life-cycle of the aphid-like pest phylloxera, and the complexity of its relationship with its host the grapevine. The effort and ingenuity that phylloxera employs to continue itself leads to a doubt that survival alone is sufficient reason. It has frequently been suggested that the reduction of life to a catalogue of facts (by science) creates this doubt, because it robs existence of its essence (which is something other than its mechanics). The part that science is said to steal is what Robert Pirsig calls Quality-the harmonious balance of things. Pirsig seems to imply that this is something inherent in things-and independent from us. A more mundane explanation is that the difference between facts and the complete reality is us-the tendency of mind to connect freely between different kinds of information. This possibility is briefly illustrated here by a myth based on the facts of phylloxera.     

Do vertebrate neural crest and cranial placodes have a common evolutionary origin?

Two embryonic tissues-the neural crest and the cranial placodes-give rise to most evolutionary novelties of the vertebrate head. These two tissues develop similarly in several respects: they originate from ectoderm at the neural plate border, give rise to migratory cells and develop into multiple cell fates including sensory neurons. These similarities, and the joint appearance of both tissues in the vertebrate lineage, may point to a common evolutionary origin of neural crest and placodes from a specialized population of neural plate border cells. However, a review of the developmental mechanisms underlying the induction, specification, migration and cytodifferentiation of neural crest and placodes reveals fundamental differences between the tissues. Taken together with insights from recent studies in tunicates and amphioxus, this suggests that neural crest and placodes have an independent evolutionary origin and that they evolved from the neural and non-neural side of the neural plate border, respectively.     

Pathophysiology of heart failure and frailty: a common inflammatory origin?

Frailty, a clinical syndrome that typically occurs in older adults, implies a reduced ability to tolerate biological stressors. Frailty accompanies many age‐related diseases but can also occur without overt evidence of end‐organ disease. The condition is associated with circulating inflammatory cytokines and sarcopenia, features that are shared with heart failure (HF). However, the biological underpinnings of frailty remain unclear and the interaction with HF is complex. Here, we describe the inflammatory pathophysiology that is associated with frailty and speculate that the inflammation that occurs with frailty shares common origins with HF. We discuss the limitations in investigating the pathophysiology of frailty due to few relevant experimental models. Leveraging current therapies for advanced HF and current known therapies to address frailty in humans may enable translational studies to better understand the inflammatory interactions between frailty and HF.     

Dreaming and schizophrenia: a common neurobiological background?

Normal waking mentation is the outcome of the combined action of both electrophysiological and neurochemical antagonistic and complementary activating and inhibitory influences occurring mainly in the cerebral cortex. The chemical ones are supported principally by acetylcholine, and noradrenaline and serotonin, respectively. During rapid eye movement (REM) sleep, the monoaminergic silence - except dopaminergic ongoing activity - disrupts this equilibrium and seems to be responsible for disturbances of mental activity characteristic of dreaming. This imbalance could cause disconnectivity of cortical areas, failure of latent inhibition and possibly the concomitant prefrontal dorsolateral deactivation. Moreover, the decrease of prefrontal dopaminergic functioning could explain the loss of reflectiveness in this sleep stage. All these phenomena are also encountered in schizophrenia. The psychotic-like mentation of dreaming (hallucinations, delusions, bizarre thought processes) could result from the disinhibition of dopamine influence in the nucleus accumbens by the noradrenergic and serotonergic local silence and/or the lifting of glutamate influence from the prefrontal cortex and hippocampus. We hypothesize that, during REM sleep, the increase of dopamine and the decrease of glutamate release observed in nucleus accumbens reach the threshold values at which psychotic disturbances arise during wakefulness. Whatever the precise mechanism, it seems that the functional state of the prefrontal cortex and nucleus accumbens is the same during dreaming sleep stage and in schizophrenia. The convergent psychological, electrophysiological, tomographic, pharmacological and neurochemical criteria of REM sleep and schizophrenia suggest that this sleep stage could become a good neurobiological model of this psychiatric disease.     

Eco-evo-devo of the lemur syndrome: did adaptive behavioral plasticity get canalized in a large primate radiation?

Background

Comprehensive explanations of behavioral adaptations rarely invoke all levels famously admonished by Niko Tinbergen. The role of developmental processes and plasticity, in particular, has often been neglected. In this paper, we combine ecological, physiological and developmental perspectives in developing a hypothesis to account for the evolution of ‘the lemur syndrome’, a combination of reduced sexual dimorphism, even adult sex ratios, female dominance and mild genital masculinization characterizing group-living species in two families of Malagasy primates.

Results

We review the different components of the lemur syndrome and compare it with similar adaptations reported for other mammals. We find support for the assertion that the lemur syndrome represents a unique set of integrated behavioral, demographic and morphological traits. We combine existing hypotheses about underlying adaptive function and proximate causation by adding a potential developmental mechanism linking maternal stress and filial masculinization, and outline an evolutionary scenario for its canalization.

Conclusions

We propose a new hypothesis linking ecological, physiological, developmental and evolutionary processes to adumbrate a comprehensive explanation for the evolution of the lemur syndrome, whose assumptions and predictions can guide diverse future research on lemurs. This hypothesis should also encourage students of other behavioral phenomena to consider the potential role of developmental plasticity in evolutionary innovation.

     

Recombination and RNA processing: a common strand?

Genetic recombination is a basic cellular process required for altering genome structure. The RecA protein of Escherichia coli has a central role in homologous recombination, and a eukaryotic protein with similar properties has been discovered in the yeast Saccharomyces cerevisiae. Unexpectedly, this RecA-like protein has additional biochemical activities, and its function may not be restricted to recombination.