Climate change reduces genetic diversity of Canada lynx at the trailing range edge

Shifts in species distributions due to environmental change may affect the spatial pattern of genetic structure within a species' range, including possible changes to the adaptive potential of populations. We investigated spatial patterns of neutral genetic diversity and differentiation at the southern edge of the Canada lynx Lynx canadensis distribution in Ontario, Canada. We analyzed provincial fur harvest records (1972–2010) and collected and genotyped lynx pelt samples (2007–2009) from 702 lynx at 14 microsatellite loci. We show that the southern range boundary of lynx in central Canada has contracted northward by > 175 km since the 1970s, and that high winter temperature, low snow depth, and low proportion of suitable habitat are strongly correlated with low neutral genetic diversity and high genetic differentiation at the trailing range edge. Our work tests fundamental ideas about species range limits and demonstrates that environmental conditions can have a marked influence on neutral genetic structure. Our results suggest that changes in environmental conditions will result in further loss of genetic diversity and possibly reduce adaptive potential in southern peripheral lynx populations.     

Hatching asynchrony that maintains egg viability also reduces brood reduction in a subtropical bird

In birds, hatching failure is pervasive and incurs an energetic and reproductive cost to breeding individuals. The egg viability hypothesis posits that exposure to warm temperatures prior to incubation decreases viability of early laid eggs and predicts that females in warm environments minimize hatching failure by beginning incubation earlier in the laying period, laying smaller clutches, or both. However, beginning incubation prior to clutch completion may incur a cost by increasing hatching asynchrony and possibly brood reduction. We examined whether Florida scrub jays (Aphelocoma coerulescens) began incubation earlier relative to clutch completion when laying larger clutches or when ambient temperatures increased, and whether variation in incubation onset influenced subsequent patterns of hatching asynchrony and brood reduction. We compared these patterns between a suburban and wildland site because site-specific differences in hatching failure match a priori predictions of the egg viability hypothesis. Females at both sites began incubation earlier relative to clutch completion when laying larger clutches and as ambient temperatures increased. Incubation onset was correlated with patterns of hatching asynchrony at both sites; however, brood reduction increased only in the suburbs, where nestling food is limiting, and only during the late nestling period. Hatching asynchrony may be an unintended consequence of beginning incubation early to minimize hatching failure of early laid eggs. Food limitation in the suburbs appears to result in increased brood reduction in large clutches that hatch asynchronously. Therefore, site-specific rates of brood reduction may be a consequence of asynchronous hatching patterns that result from parental effort to minimize hatching failure in first-laid eggs. This illustrates how anthropogenic change, such as urbanization, can lead to loss of fitness when animals use behavioral strategies intended to maximize fitness in natural landscapes.     

IL-22 is induced by S100/calgranulin and impairs cholesterol efflux in macrophages by downregulating ABCG1

S100A8/9 and S100A12 are emerging biomarkers for disease activity of autoimmune and cardiovascular diseases. We demonstrated previously that S100A12 accelerates atherosclerosis accompanied by large cholesterol deposits in atherosclerotic lesions of apoE-null mice. The objective of this study was to ascertain whether S100/calgranulin influences cholesterol homeostasis in macrophages. Peritoneal macrophages from transgenic mice expressing human S100A8/9 and S100A12 in myeloid cells [human bacterial artificial chromosome (hBAC)/S100] have increased lipid content and reduced ABCG1 expression and [³H]cholesterol efflux compared with WT littermates. This was associated with a 6-fold increase in plasma interleukin (IL)-22 and increased IL-22 mRNA in splenic T cells. These findings are mediated by the receptor for advanced glycation endproducts (RAGE), because hBAC/S100 mice lacking RAGE had normal IL-22 expression and normal cholesterol efflux. In vitro, recombinant IL-22 reduced ABCG1 expression and [³H]cholesterol efflux in THP-1 macrophages, while recombinant S100A12 had no effect on ABCG1 expression. In conclusion, S100/calgranulin has no direct effect on cholesterol efflux in macrophages, but rather promotes the secretion of IL-22, which then directly reduces cholesterol efflux in macrophages by decreasing the expression of ABCG1.     

BDNF and Huntingtin protein modifications by manganese: implications for striatal medium spiny neuron pathology in manganese neurotoxicity

High levels of manganese (Mn) exposure decrease striatal medium spiny neuron (MSN) dendritic length and spine density, but the mechanism(s) are not known. The Huntingtin (HTT) gene has been functionally linked to cortical brain‐derived neurotrophic factor (BDNF) support of striatal MSNs via phosphorylation at serine 421. In Huntington's disease, pathogenic CAG repeat expansions of HTT decrease synthesis and disrupt transport of cortical–striatal BDNF, which may contribute to disease, and Mn is a putative environmental modifier of Huntington's disease pathology. Thus, we tested the hypothesis that changes in MSN dendritic morphology Mn due to exposure are associated with decreased BDNF levels and alterations in Htt protein. We report that BDNF levels are decreased in the striatum of Mn‐exposed non‐human primates and in the cerebral cortex and striatum of mice exposed to Mn. Furthermore, proBDNF and mature BDNF concentrations in primary cortical and hippocampal neuron cultures were decreased by exposure to Mn confirming the in vivo findings. Mn exposure decreased serine 421 phosphorylation of Htt in cortical and hippocampal neurons and increased total Htt levels. These data strongly support the hypothesis that Mn‐exposure‐related MSN pathology is associated with decreased BDNF trophic support via alterations in Htt.

     

Future eating and country keeping: what role has environmental history in the management of biodiversity?

In order to understand and moderate the effects of the accelerating rate of global environmental change land managers and ecologists must not only think beyond their local environment but also put their problems into a historical context. It is intuitively obvious that historians should be natural allies of ecologists and land managers as they struggle to maintain biodiversity and landscape health. Indeed, ‘environmental history’ is an emerging field where the previously disparate intellectual traditions of ecology and history intersect to create a new and fundamentally interdisciplinary field of inquiry. Environmental history is rapidly becoming an important field displacing many older environmentally focused academic disciplines as well as capturing the public imagination. By drawing on Australian experience I explore the role of ‘environmental history’ in managing biodiversity. First I consider some of the similarities and differences of the ecological and historical approaches to the history of the environment. Then I review two central questions in Australian environment history: landscape‐scale changes in woody vegetation cover since European settlement and the extinction of the marsupials in both historical and pre‐historical time. These case studies demonstrate that environmental historians can reach conflicting interpretations despite using essentially the same data. The popular success of some environmental histories hinges on the fact that they narrate a compelling story concerning human relationships and human value judgements about landscape change. Ecologists must learn to harness the power of environmental history narratives to bolster land management practices designed to conserve biological heritage. They can do this by using various currently popular environmental histories as a point of departure for future research, for instance by testing the veracity of competing interpretations of landscape‐scale change in woody vegetation cover. They also need to learn how to write parables that communicate their research findings to land managers and the general public. However, no matter how sociologically or psychologically satisfying a particular environmental historical narrative might be, it must be willing to be superseded with new stories that incorporate the latest research discoveries and that reflects changing social values of nature. It is contrary to a rational and publicly acceptable approach to land management to read a particular story as revealing the absolute truth.     

Plk1 Inhibition Causes Post-Mitotic DNA Damage and Senescence in a Range of Human Tumor Cell Lines

Plk1 is a checkpoint protein whose role spans all of mitosis and includes DNA repair, and is highly conserved in eukaryotes from yeast to man. Consistent with this wide array of functions for Plk1, the cellular consequences of Plk1 disruption are diverse, spanning delays in mitotic entry, mitotic spindle abnormalities, and transient mitotic arrest leading to mitotic slippage and failures in cytokinesis. In this work, we present the in vitro and in vivo consequences of Plk1 inhibition in cancer cells using potent, selective small-molecule Plk1 inhibitors and Plk1 genetic knock-down approaches. We demonstrate for the first time that cellular senescence is the predominant outcome of Plk1 inhibition in some cancer cell lines, whereas in other cancer cell lines the dominant outcome appears to be apoptosis, as has been reported in the literature. We also demonstrate strong induction of DNA double-strand breaks in all six lines examined (as assayed by γH2AX), which occurs either during mitotic arrest or mitotic-exit, and may be linked to the downstream induction of senescence. Taken together, our findings expand the view of Plk1 inhibition, demonstrating the occurrence of a non-apoptotic outcome in some settings. Our findings are also consistent with the possibility that mitotic arrest observed as a result of Plk1 inhibition is at least partially due to the presence of unrepaired double-strand breaks in mitosis. These novel findings may lead to alternative strategies for the development of novel therapeutic agents targeting Plk1, in the selection of biomarkers, patient populations, combination partners and dosing regimens.     

Assessing the Relationship between Vector Indices and Dengue Transmission: A Systematic Review of the Evidence

Background

Despite doubts about methods used and the association between vector density and dengue transmission, routine sampling of mosquito vector populations is common in dengue-endemic countries worldwide. This study examined the evidence from published studies for the existence of any quantitative relationship between vector indices and dengue cases.

Methodology/Principal Findings

From a total of 1205 papers identified in database searches following Cochrane and PRISMA Group guidelines, 18 were included for review. Eligibility criteria included 3-month study duration and dengue case confirmation by WHO case definition and/or serology.A range of designs were seen, particularly in spatial sampling and analyses, and all but 3 were classed as weak study designs. Eleven of eighteen studies generated Stegomyia indices from combined larval and pupal data. Adult vector data were reported in only three studies. Of thirteen studies that investigated associations between vector indices and dengue cases, 4 reported positive correlations, 4 found no correlation and 5 reported ambiguous or inconclusive associations. Six out of 7 studies that measured Breteau Indices reported dengue transmission at levels below the currently accepted threshold of 5.

Conclusions/Significance

There was little evidence of quantifiable associations between vector indices and dengue transmission that could reliably be used for outbreak prediction. This review highlighted the need for standardized sampling protocols that adequately consider dengue spatial heterogeneity. Recommendations for more appropriately designed studies include: standardized study design to elucidate the relationship between vector abundance and dengue transmission; adult mosquito sampling should be routine; single values of Breteau or other indices are not reliable universal dengue transmission thresholds; better knowledge of vector ecology is required.     

Protein Thermodynamics Can Be Predicted Directly from Biological Growth Rates

Life on Earth is capable of growing from temperatures well below freezing to above the boiling point of water, with some organisms preferring cooler and others hotter conditions. The growth rate of each organism ultimately depends on its intracellular chemical reactions. Here we show that a thermodynamic model based on a single, rate-limiting, enzyme-catalysed reaction accurately describes population growth rates in 230 diverse strains of unicellular and multicellular organisms. Collectively these represent all three domains of life, ranging from psychrophilic to hyperthermophilic, and including the highest temperature so far observed for growth (122°C). The results provide credible estimates of thermodynamic properties of proteins and obtain, purely from organism intrinsic growth rate data, relationships between parameters previously identified experimentally, thus bridging a gap between biochemistry and whole organism biology. We find that growth rates of both unicellular and multicellular life forms can be described by the same temperature dependence model. The model results provide strong support for a single highly-conserved reaction present in the last universal common ancestor (LUCA). This is remarkable in that it means that the growth rate dependence on temperature of unicellular and multicellular life forms that evolved over geological time spans can be explained by the same model.