Species loss and gain in communities under future climate change: consequences for functional diversity

It is anticipated that anthropogenic climate change will lead to substantial reassembly within communities in coming decades as individual species shift their ranges to track optimal conditions for growth and survival. As species are lost and gained in communities, what are the consequences for functional trait diversity? Functional traits are the characteristics of species that affect individual performance and provide the vital link between biodiversity at the species level and ecosystem function. We investigated how projected changes in species richness in plant communities under climate change scenarios for the decade 2050 will affect the distribution and diversity of five functional traits. We aggregated range change projections made in Maxent for the decade 2050 across all species in the regional pool of littoral rainforest vines in eastern Australia (n = 163 species). The effect of richness changes on trait diversity was assessed in nine rainforest reserves along the east coast of Australia. Although richness was predicted to significantly decline across all communities, functional diversity remained stable, indicating a decoupling in response to climate change at these two different levels of biological organization. A high degree of redundancy in trait composition in communities may buffer against the loss of function in these plant communities. Scaling‐up our understanding of the impact of climate change from the species level to communities is a critical step towards developing conservation strategies aimed at preserving ecosystem function.     

Human sleep‐wake cycles in the high arctic: Effects of unusual photoperiodicity in a natural setting

Abstract

Studies of human circadian rhythms are typically conducted in artificial environments that are low in ecological validity. In the current study, six subjects and the field director lived in temporal isolation in a completely natural environment with constant daylight (a high Arctic research camp) for six weeks. Detailed daily sleep logs were kept. In keeping with past findings, five of the six subjects developed a free‐running sleep‐wake cycle longer than 24 hours. Unlike past results, the isolated subjects did not exhibit any synchronicity in their rhythms. There was a high degree of intersubject variability in circadian patterns. The findings have important implications for the comparison of the results of laboratory and field investigations of sleep‐wake cycles.     

Distinct roles for ROCK1 and ROCK2 in the regulation of cell detachment

This study, using mouse embryonic fibroblast (MEF) cells derived from ROCK1^−/− and ROCK2^−/− mice, is designed to dissect roles for ROCK1 and ROCK2 in regulating actin cytoskeleton reorganization induced by doxorubicin, a chemotherapeutic drug. ROCK1^−/− MEFs exhibited improved actin cytoskeleton stability characterized by attenuated periphery actomyosin ring formation and preserved central stress fibers, associated with decreased myosin light chain 2 (MLC2) phosphorylation but preserved cofilin phosphorylation. These effects resulted in a significant reduction in cell shrinkage, detachment, and predetachment apoptosis. In contrast, ROCK2^−/− MEFs showed increased periphery membrane folding and impaired cell adhesion, associated with reduced phosphorylation of both MLC2 and cofilin. Treatment with inhibitor of myosin (blebbistatin), inhibitor of actin polymerization (cytochalasin D), and ROCK pan-inhibitor (Y27632) confirmed the contributions of actomyosin contraction and stress fiber instability to stress-induced actin cytoskeleton reorganization. These results support a novel concept that ROCK1 is involved in destabilizing actin cytoskeleton through regulating MLC2 phosphorylation and peripheral actomyosin contraction, whereas ROCK2 is required for stabilizing actin cytoskeleton through regulating cofilin phosphorylation. Consequently, ROCK1 and ROCK2 can be functional different in regulating stress-induced stress fiber disassembly and cell detachment.     

Blocking Apoptotic Signaling Rescues Axon Guidance in Netrin Mutants

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Behavioral and transcriptome alterations in male and female mice with postnatal deletion of TrkB in dorsal striatal medium spiny neurons

Background

The high affinity tyrosine kinase receptor, TrkB, is the primary receptor for brain derived neurotrophic factor (BDNF) and plays an important role in development, maintenance and plasticity of the striatal output medium size spiny neuron. The striatal BDNF/TrkB system is thereby implicated in many physiologic and pathophysiologic processes, the latter including mood disorders, addiction, and Huntington’s disease. We crossed a mouse harboring a transgene directing cre-recombinase expression primarily to postnatal, dorsal striatal medium spiny neurons, to a mouse containing a floxed TrkB allele (fB) mouse designed for deletion of TrkB to determine its role in the adult striatum.

Results

We found that there were sexually dimorphic alterations in behaviors in response to stressful situations and drugs of abuse. Significant sex and/or genotype differences were found in the forced swim test of depression-like behaviors, anxiety-like behaviors on the elevated plus maze, and cocaine conditioned reward. Microarray analysis of dorsal striatum revealed significant dysregulation in individual and groups of genes that may contribute to the observed behavioral responses and in some cases, represent previously unidentified downstream targets of TrkB.

Conclusions

The data point to a set of behaviors and changes in gene expression following postnatal deletion of TrkB in the dorsal striatum distinct from those in other brain regions.

     

The PathoChip,a functional gene array for assessing pathogenic properties of diverse microbial communities

Pathogens present in the environment pose a serious threat to human, plant and animal health as evidenced by recent outbreaks. As many pathogens can survive and proliferate in the environment, it is important to understand their population dynamics and pathogenic potential in the environment. To assess pathogenic potential in diverse habitats, we developed a functional gene array, the PathoChip, constructed with key virulence genes related to major virulence factors, such as adherence, colonization, motility, invasion, toxin, immune evasion and iron uptake. A total of 3715 best probes were selected from 13 virulence factors, covering 7417 coding sequences from 1397 microbial species (2336 strains). The specificity of the PathoChip was computationally verified, and approximately 98% of the probes provided specificity at or below the species level, proving its excellent capability for the detection of target sequences with high discrimination power. We applied this array to community samples from soil, seawater and human saliva to assess the occurrence of virulence genes in natural environments. Both the abundance and diversity of virulence genes increased in stressed conditions compared with their corresponding controls, indicating a possible increase in abundance of pathogenic bacteria under environmental perturbations such as warming or oil spills. Statistical analyses showed that microbial communities harboring virulence genes were responsive to environmental perturbations, which drove changes in abundance and distribution of virulence genes. The PathoChip provides a useful tool to identify virulence genes in microbial populations, examine the dynamics of virulence genes in response to environmental perturbations and determine the pathogenic potential of microbial communities.     

Current approaches to native woodland restoration in Scotland

Summary

A large number of projects have recently been initiated in Scotland aiming to restore native woodland, which are being undertaken by a variety of organisations, often in partnership, with environmental NGOs playing a leading role. The objectives, constraints and methodologies of these projects are critically reviewed, partly through a questionnaire survey. Most aim to restore ‘natural’ woodland, but the lack of appropriate reference ecosystems and uncertainty about the characteristics of the original forest hinder the development of precise objectives, and consequently the criteria for success are poorly defined. Most projects face major practical constraints, particularly browsing by herbivores and invasion by exotic species, indicating that they will require long-term management interventions. Most woodlands are isolated from other woodlands, which threatens their long-term viability, restricting colonisation by woodland organisms. Greater reference to ecological theory in practical restoration projects such as these would enable objectives to be defined with more precision, encourage a greater emphasis on ecological processes rather than community composition, and improve management plans through use of predictive tools. In particular, the integration of woodlands into habitat networks, increasing ecological connectivity between woodland fragments, is considered essential to ensure success in the long term.     

TGF-b Superfamily Cytokine MIC-1/GDF15 Is a Physiological Appetite and Body Weight Regulator

The TGF-b superfamily cytokine MIC-1/GDF15 circulates in all humans and when overproduced in cancer leads to anorexia/cachexia, by direct action on brain feeding centres. In these studies we have examined the role of physiologically relevant levels of MIC-1/GDF15 in the regulation of appetite, body weight and basal metabolic rate. MIC-1/GDF15 gene knockout mice (MIC-1^−/−) weighed more and had increased adiposity, which was associated with increased spontaneous food intake. Female MIC-1^−/− mice exhibited some additional alterations in reduced basal energy expenditure and physical activity, possibly owing to the associated decrease in total lean mass. Further, infusion of human recombinant MIC-1/GDF15 sufficient to raise serum levels in MIC-1^−/− mice to within the normal human range reduced body weight and food intake. Taken together, our findings suggest that MIC-1/GDF15 is involved in the physiological regulation of appetite and energy storage.     

Genetic Variants in Vitamin D Pathway Genes and Risk of Pancreas Cancer; Results from a Population-Based Case-Control Study in Ontario,Canada

Recent studies of 25-hydroxyvitamin D (25(OH)D) levels and pancreas cancer have suggested a potential role of the vitamin D pathway in the etiology of this fatal disease. Variants in vitamin-D related genes are known to affect 25(OH)D levels and function and it is unknown if these variants may influence pancreatic cancer risk. The association between 87 single nucleotide polymorphisms (SNPs) in 11 genes was evaluated within the Ontario Pancreas Cancer Study, a population-based case-control study. Pancreatic cancer cases with pathology confirmed adenocarcinoma were identified from the Ontario Cancer Registry (n = 628) and controls were identified through random digit dialing (n = 1193). Age and sex adjusted odds ratios (OR) and 95% confidence intervals (CI) were estimated by multivariate logistic regression. SNPs in the CYP24A1, CYP2R1, calcium sensing receptor (CASR), vitamin D binding protein (GC), retinoid X receptor-alpha (RXRA) and megalin (LRP2) genes were significantly associated with pancreas cancer risk. For example, pancreas cancer risk was inversely associated with CYP2R1 rs10741657 (AA versus GG, OR = 0.70; 95%CI: 0.51–0.95) and positively with CYP24A1 rs6127119 (TT versus CC. OR = 1.94; 95%CI: 1.28–2.94). None of the associations were statistically significant after adjustment for multiple comparisons. Vitamin D pathway gene variants may be associated with pancreas cancer risk and future studies are needed to understand the possible role of vitamin D in tumorigenesis and may have implications for cancer-prevention strategies.