A shift in habitat use patterns of brown trout (Salmo trutta): A behavioural response to macrophyte removal

Mass development of macrophytes is an increasing problem worldwide and they are frequently removed where they are in conflict with local waterway users. Yet, macrophytes can provide important refuge and nursery habitats for fish. Little is known about the consequences of macrophyte removal for fish behavioural space use and habitat selection. We hypothesised that macrophyte removal would affect brown trout (Salmo trutta) movement during the partial removal of the aquatic plant Juncus bulbosus (L.) in an oligotrophic impounded Norwegian river.We tagged 94 brown trout and tracked them using passive acoustic telemetry for 10 months and mapped the cover of J. bulbosus. Trout behavioural patterns were quantified as space use (utilisation areas 50% and 95%) which was linked to habitat use and selection for J. bulbosus. Removal of J. bulbosus influenced space use of brown trout by reducing the core utilisation area by 22%. Habitat use and selection were likewise influenced by removal with increased use and selection of areas with low J. bulbosus cover (25–75%). Finally, diurnal differences in space use and habitat use were found, with 19% larger utilisation areas at night and higher use of areas with low J. bulbosus during daytime. Yet, all effect sizes were relatively small compared to the size of the study area. This research provides a detailed case study on the effects of macrophyte removal on fish behavioural patterns in a section of a large Norwegian river with macrophyte mass development. We found no large effects of removal on trout behaviour but noted an increased use of areas with low macrophyte cover. This research is relevant for water managers and policy makers of freshwater conservation and provides a template for using acoustic telemetry to study the effects of macrophyte removal on fish.publishedVersio

Decline of nucleotide excision repair capacity in aging Caenorhabditis elegans

Repair of UVC-induced DNA damage in Caenorhabditis elegans is similar kinetically and genetically to repair in humans, and it slows significantly in aging C. elegans

Mitochondria, Energetics, Epigenetics, and Cellular Responses to Stress

Background: Cells respond to environmental stressors through several key pathways, including response to reactive oxygen species (ROS), nutrient and ATP sensing, DNA damage response (DDR), and epigenetic alterations. Mitochondria play a central role in these pathways not only through energetics and ATP production but also through metabolites generated in the tricarboxylic acid cycle, as well as mitochondria–nuclear signaling related to mitochondria morphology, biogenesis, fission/fusion, mitophagy, apoptosis, and epigenetic regulation. Objectives: We investigated the concept of bidirectional interactions between mitochondria and cellular pathways in response to environmental stress with a focus on epigenetic regulation, and we examined DNA repair and DDR pathways as examples of biological processes that respond to exogenous insults through changes in homeostasis and altered mitochondrial function. Methods: The National Institute of Environmental Health Sciences sponsored the Workshop on Mitochondria, Energetics, Epigenetics, Environment, and DNA Damage Response on 25–26 March 2013. Here, we summarize key points and ideas emerging from this meeting. Discussion: A more comprehensive understanding of signaling mechanisms (cross-talk) between the mitochondria and nucleus is central to elucidating the integration of mitochondrial functions with other cellular response pathways in modulating the effects of environmental agents. Recent studies have highlighted the importance of mitochondrial functions in epigenetic regulation and DDR with environmental stress. Development and application of novel technologies, enhanced experimental models, and a systems-type research approach will help to discern how environmentally induced mitochondrial dysfunction affects key mechanistic pathways. Conclusions: Understanding mitochondria–cell signaling will provide insight into individual responses to environmental hazards, improving prediction of hazard and susceptibility to environmental stressors. Citation: Shaughnessy DT, McAllister K, Worth L, Haugen AC, Meyer JN, Domann FE, Van Houten B, Mostoslavsky R, Bultman SJ, Baccarelli AA, Begley TJ, Sobol RW, Hirschey MD, Ideker T, Santos JH, Copeland WC, Tice RR, Balshaw DM, Tyson FL. 2014. Mitochondria, energetics, epigenetics, and cellular responses to stress. Environ Health Perspect 122:1271–1278; http://dx.doi.org/10.1289/ehp.140841

Altered gene expression and DNA damage in peripheral blood cells from Friedreich's ataxia patients: Cellular model of pathology

The neurodegenerative disease Friedreich's ataxia (FRDA) is the most common autosomal-recessively inherited ataxia and is caused by a GAA triplet repeat expansion in the first intron of the frataxin gene. In this disease, transcription of frataxin, a mitochondrial protein involved in iron homeostasis, is impaired, resulting in a significant reduction in mRNA and protein levels. Global gene expression analysis was performed in peripheral blood samples from FRDA patients as compared to controls, which suggested altered expression patterns pertaining to genotoxic stress. We then confirmed the presence of genotoxic DNA damage by using a gene-specific quantitative PCR assay and discovered an increase in both mitochondrial and nuclear DNA damage in the blood of these patients (p<0.0001, respectively). Additionally, frataxin mRNA levels correlated with age of onset of disease and displayed unique sets of gene alterations involved in immune response, oxidative phosphorylation, and protein synthesis. Many of the key pathways observed by transcription profiling were downregulated, and we believe these data suggest that patients with prolonged frataxin deficiency undergo a systemic survival response to chronic genotoxic stress and consequent DNA damage detectable in blood. In conclusion, our results yield insight into the nature and progression of FRDA, as well as possible therapeutic approaches. Furthermore, the identification of potential biomarkers, including the DNA damage found in peripheral blood, may have predictive value in future clinical trials

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

Becoming aWARE: The Development of a Web-Based Tool for Autism Research and the Environment

A sharp rise in autism spectrum disorder (ASD) prevalence estimates, beginning in the 1990s, suggested factors additional to genetics were at play. This stimulated increased research investment in nongenetic factors, including the study of environmental chemical exposures, diet, nutrition, lifestyle, social factors, and maternal medical conditions. Consequently, both peer- and non-peer-reviewed bodies of evidence investigating environmental contributors to ASD etiology have grown significantly. The heterogeneity in the design and conduct of this research results in an inconclusive and unwieldy ‘virtual stack’ of publications. We propose to develop a Web-based tool for Autism Research and the Environment (aWARE) to comprehensively aggregate and assess these highly variable and often conflicting data. The interactive aWARE tool will use an approach for the development of systematic evidence maps (SEMs) to identify and display all available relevant published evidence, enabling users to explore multiple research questions within the scope of the SEM. Throughout tool development, listening sessions and workshops will be used to seek perspectives from the broader autism community. New evidence will be indexed in the tool annually, which will serve as a living resource to investigate the association between environmental factors and ASD

Top 20 central nodes representing perturbed neighborhoods, identified by Cytoscape

<p><b>Copyright information:</b></p><p>Taken from "Decline of nucleotide excision repair capacity in aging "</p><p>http://genomebiology.com/2007/8/5/R70</p><p>Genome Biology 2007;8(5):R70-R70.</p><p>Published online 1 May 2007</p><p>PMCID:PMC1929140.</p><p></p> Green indicates downregulation, and red indicates upregulation of the gene/node in aging (6 days after L4) versus young (1 day after L4) nematodes; darker shades indicate greater alteration. Blue borders indicate genes that were significantly different in expression individually in aging compared with young adults (< 0.05). Nodes that are grouped into the gray cluster do not fall into a common Gene Ontology. Additional data file 4 (parts A and B) provides additional information about each of the nodes (genes) and the associated neighborhoods

Marked variation in susceptibility to UVC-induced DNA damage in different life stages of

<p><b>Copyright information:</b></p><p>Taken from "Decline of nucleotide excision repair capacity in aging "</p><p>http://genomebiology.com/2007/8/5/R70</p><p>Genome Biology 2007;8(5):R70-R70.</p><p>Published online 1 May 2007</p><p>PMCID:PMC1929140.</p><p></p> The UVC dose and life stage both had significant effects on induction of nuclear and mitochondrial lesions (< 0.0001 for main effects of both), but no difference was observed between the nuclear and mitochondrial genomes (= 0.9218 for main effect of genome) in a three-factor analysis of variance. All life stages and doses were statistically distinct from each other (< 0.0001 in all cases, Fisher's protected least significant difference [FPLSD]), except the adult stages (> 0.05 for all pair-wise comparisons, FPLSD). = 3 for each column; error bars represent standard errors of the mean