Fluctuating asymmetry as an indicator of fitness: can we bridge the gap between studies?

There is growing evidence from both experimental and non-experimental studies that fluctuating asymmetry does not consistently index stress or fitness. The widely held--yet poorly substantiated--belief that fluctuating asymmetry can act as a universal measure of developmental stability and predictor of stress-mediated changes in fitness, therefore staggers. Yet attempts to understand why the reported relationships between fluctuating asymmetry, stress and fitness are so heterogeneous--i.e. whether the associations are truly weak or non-existent or whether they become confounded during different stages of the analytical pathways remain surprisingly scarce. Hence, we attempt to disentangle these causes, by reviewing the various statistical and conceptual factors that are suspected to confound potential relationships between fluctuating asymmetry, stress and fitness. Two main categories of factors are discerned: those associated with the estimation of developmental stability through fluctuating asymmetry and those associated with the effects of genotype and environment on developmental stability. Next, we describe a series of statistical tools that have recently been developed to help reduce this noise. We argue that the current lack of a theoretical framework that predicts if and when relationships with developmental stability can be expected, urges for further theoretical and empirical research, such as on the genetic architecture of developmental stability in stressed populations. If the underlying developmental mechanisms are better understood, statistical patterns of asymmetry variation may become a biologically meaningful tool.     

Developmental signaling: Does it bridge the gap between cilia dysfunction and renal cystogenesis?

For more than a decade, evidence has accumulated linking dysfunction of primary cilia to renal cystogenesis, yet molecular mechanisms remain undefined. The pathogenesis of renal cysts is complex, involving multiple cellular aberrations and signaling pathways. Adding to this complexity, primary cilia exhibit multiple roles in a context‐dependent manner. On renal epithelial cells, primary cilia act as mechanosensors and trigger extracellular Ca²⁺ influx in response to laminar fluid flow. During mammalian development, primary cilia mediate the Hedgehog (Hh), Wnt, and Notch pathways, which control cell proliferation and differentiation, and tissue morphogenesis. Further, experimental evidence suggests the developmental state of the kidney strongly influences renal cystic disease. Thus, we review evidence for regulation of Ca²⁺ and cAMP, key molecules in renal cystogenesis, at the primary cilium, the role of Hh, Wnt, and Notch signaling in renal cystic disease, and the interplay between these developmental pathways and Ca²⁺ signaling. Indeed if these developmental pathways influence renal cystogenesis, these may represent novel therapeutic targets that can be integrated into a combination therapy for renal cystic disease. Birth Defects Research (Part C) 102:159–173, 2014. © 2014 Wiley Periodicals, Inc.     

Early warning signals of regime shifts for aquatic systems: Can experiments help to bridge the gap between theory and real-world application?

Early-warning signals of a regime shift (EWS) indicate, for a wide range of systems, if a tipping-point is being approached. In ecology, EWS are well established from a theoretical perspective but are far from unequivocal when applied to field data. The gap between theory and application is caused by a set of limitations, like the lack of coherence between different EWS, data acquisition issues, and false results. Experiments assessing EWS may provide an empirical mechanistic understanding of why an EWS was observed (or failed to be observed), which often cannot be elucidated by simple computational modeling or pure environmental data. Here we focused on aquatic experiments to explore to what extent the existing EWS experiments can bridge the gap between the theory and real-world application. For that, we used the Thomson-ISI Web of Science© database to retrieve EWS experiments executed before early-2020, detailing their experimental designs and each EWS assessed. Success rates - correct anticipation of tipping points – were around 70% for the most used EWS (assessment of autocorrelation, variance, recovery, and shape of the distribution using abundance, Chlorophyll-a, Phycocyanin, and dissolved oxygen data). Yet, no EWS showed to be 100% reliable, and their use demands cautious interpretation. As a rule, we observed that experiments were not designed to tackle issues encountered in real-world situations. They lack a deep mechanistic understanding of why, when, and how an EWS was observed or not. When experiments did aim to assess issues encountered in the real world, the experimental designs were often of low ecological significance. We also investigated the relationship between sampling and the success rate of EWS, observing that the sampling regime might have to be tailor-made towards specific monitoring objectives. Moreover, experiments have taught us that the use of EWS can be more versatile than expected, going from monitoring the extinction of single populations to the anticipation of transient regime shifts. Most of the experiments presented here supported empirical proof of the existence of EWS in aquatic systems. Still, to bridge the gap between theory and application, experiments will have to move closer to real-world conditions and better support a mechanistic understanding of why EWS may succeed or fail to anticipate a regime shift. For that, we provide six elements to take into account when designing experiments that could enhance the capabilities of EWS to go beyond the stage of proof-of-concept.     

The phylogenetic relationships of the shags and cormorants: can sequence data resolve a disagreement between behavior and morphology?

Taxonomic arrangements for the cormorants and shags (Phalacrocoracidae) had varied greatly until two quite similar arrangements, one based on behavior and the other on osteological characters, became the basis for current thought on the evolutionary relationships of these birds. The terms cormorant and shag, which had previously been haphazardly applied to members of the group, became the vernacular terms for the two major subdivisions within this family. The two taxonomies differ in places, however, with the behavioral taxonomy placing several species within the shags and the osteological taxonomy and phylogeny grouping those species (as the marine cormorants) and placing them within the cormorants. In an attempt to resolve the differences in the relationships hypothesized by behavior and morphology, we sequenced three mitochondrial genes (12S, ATPase 6, and ATPase 8). Initial equally weighted parsimony trees differed slightly from our two weighted parsimony trees, one of which was also our maximum-likelihood tree. Many of the branches within our trees were well supported, but some sections of the phylogeny proved difficult to resolve with confidence. Our sequence trees differ substantially from the morphological phylogeny and show that neither the shags nor the cormorants are monophyletic, but form an intermingled group. Some of the groups supported by both the behavioral and the morphological taxonomies (e.g., the cliff shags, Stictocarbo) appear to be polyphyletic. Conversely, the monophyly of the blue-eyed shags, a traditional group that the osteological analysis had found to be paraphyletic, was supported by the sequence data. Until more taxa are sampled and a fully robust phylogeny is obtained, a conservative approach accepting a single genus, Phalacrocorax, for the shags and cormorants is recommended.     

What can we learn about ecology and evolution from the fossil record?

The increased application of abundance data embedded within a more detailed and precise environmental context is enabling paleontologists to explore more rigorously the dynamics and underlying processes of ecological and evolutionary change in deep time. Several recent findings are of special theoretical interest. Community membership is commonly more stable and persistent than expected by chance, even in the face of the extreme environmental changes of the Ice Ages, and major evolutionary novelties commonly lie dormant for tens of millions of years before the ecological explosions of the clades that possess them. As we discuss here, questions such as these cannot be adequately addressed without the use of the fossil record.     

Visfatin: the missing link between intra-abdominal obesity and diabetes?

Human obesity-related diabetes and the accompanying metabolic disorders have been specifically linked to increased visceral adipose tissue mass. Understanding the differences in biology of the two human fat depots (visceral and subcutaneous) might hold the key to therapeutic strategies aimed at reducing obesity-induced insulin resistance and alleviating symptoms of the metabolic syndrome. Visfatin (pre-B-cell colony-enhancing factor, PBEF) is a novel adipokine that appears to be preferentially produced by visceral adipose tissue and has insulin-mimetic actions. Could this molecule hold the key to future treatments for type 1 and 2 diabetes? This article discusses the pros and cons of visfatin action and how it might affect future therapeutic strategies.     

Polyoxovanadates: The missing link between simple paramagnets and bulk magnets?

Oxovanadium clusters provide novel examples of large magnetic clusters, which may showin nuce the typical behavior of bulk magnetic materials.The paper reviews the magnetic properties of V₁₅, comprising fifteen oxovanadium(IV); V₁₄, comprising fourteen oxovanadium(IV); V₃₊₁, comprising three localized oxovanadium(IV), six localized oxovanadium(V), and one oxovanadium(IV) delocalized over three sites; V₄₊₂ and V₄₊₄ which comprise four localized and two and four delocalized oxovanadium(IV), respectively. The different observed magnetic behaviors are discussed on the basis of several models of different sophistication.     

The gut microbiota-artery axis: A bridge between dietary lipids and atherosclerosis?

Atherosclerotic cardiovascular disease is one of the major leading global causes of death. Growing evidence has demonstrated that gut microbiota (GM) and its metabolites play a pivotal role in the onset and progression of atherosclerosis (AS), now known as GM-artery axis. There are interactions between dietary lipids and GM, which ultimately affect GM and its metabolites. Given these two aspects, the GM-artery axis may play a mediating role between dietary lipids and AS. Diets rich in saturated fatty acids (SFAs), omega-6 polyunsaturated fatty acids (n-6 PUFAs), industrial trans fatty acids (TFAs), and cholesterol can increase the levels of atherogenic microbes and metabolites, whereas monounsaturated fatty acids (MUFAs), ruminant TFAs, and phytosterols (PS) can increase the levels of antiatherogenic microbes and metabolites. Actually, dietary phosphatidylcholine (PC), sphingomyelin (SM), and omega-3 polyunsaturated fatty acids (n-3 PUFAs) have been demonstrated to affect AS via the GM-artery axis. Therefore, that GM-artery axis acts as a communication bridge between dietary lipids and AS. Herein, we will describe the molecular mechanism of GM-artery axis in AS and discuss the complex interactions between dietary lipids and GM. In particular, we will highlight the evidence and potential mechanisms of dietary lipids affecting AS via GM-artery axis.     

Obligate biotroph parasitism: can we link genomes to lifestyles?

Although the oomycetes and fungi are evolutionarily very distantly related, both taxa evolved biotrophy on plant hosts several times independently, giving rise to rust- and mildew-like phenotypes. Differences in host colonization and adaptation may be reflected in genome size and by gain and loss of genes. In this opinion article we combine classical knowledge with recently sequenced pathogen genomes and present new hypotheses about the convergent evolution that led to these two distinct phenotypes in obligate biotrophs.     

The principles and practice of human evolution research: Are we asking questions that can be answered?

The research agenda of paleoanthropology involves many topics and methodologies. Fossil specimens are allocated to species, and those species are assigned to the hominin clade. After that we want to know how they are related to each other, what they ate, how much they weighed, how smart they were, etc. We also want to know about the origin of particular attributes of hominins, such as our delayed growth and development, bipedalism, and language. The data available to answer these complex questions are confounded by fragmentary fossil specimens, small sample sizes, limited opportunities for controlled experimentation, and the inherent limitations of historical data. Also, because many traits are effectively unique to hominins, even observational comparative studies are inevitably limited in what they can tell us, if not impossible to conduct. We explore how these limitations should, but often do not, constrain the questions that paleoanthropologists should attempt to answer.     

Floating between the poles of pathology and protection: can we pin down the granuloma in tuberculosis?

The granuloma in tuberculosis (TB), referred to as the tubercle, is a lesion containing multiple cell types and is the one definite hallmark of this disease. A number of tubercle phenotypes are seen during infection yet how these contribute to development of TB remains unclear. Here we highlight recent results using diverse models of tubercle development as well as recent findings from studies of human TB in an attempt to illustrate the plasticity of the tubercle and to place it between the poles of pathology and protection. Such insights could lead to future interventions to address TB as a global health issue.     

Axon-glial disruption: the link between vascular disease and Alzheimer's disease?

Vascular risk factors play a critical role in the development of cognitive decline and AD (Alzheimer's disease), during aging, and often result in chronic cerebral hypoperfusion. The neurobiological link between hypoperfusion and cognitive decline is not yet defined, but is proposed to involve damage to the brain's white matter. In a newly developed mouse model, hypoperfusion, in isolation, produces a slowly developing and diffuse damage to myelinated axons, which is widespread in the brain, and is associated with a selective impairment in working memory. Cerebral hypoperfusion, an early event in AD, has also been shown to be associated with white matter damage and notably an accumulation of amyloid. The present review highlights some of the published data linking white matter disruption to aging and AD as a result of vascular dysfunction. A model is proposed by which chronic cerebral hypoperfusion, as a result of vascular factors, results in both the generation and accumulation of amyloid and injury to white matter integrity, resulting in cognitive impairment. The generation of amyloid and accumulation in the vasculature may act to perpetuate further vascular dysfunction and accelerate white matter pathology, and as a consequence grey matter pathology and cognitive decline.