No difference in 1RM strength and muscle activation during the barbell chest press on a stable and unstable surface

Exercise or Swiss balls are increasingly being used with conventional resistance exercises. There is little evidence supporting the efficacy of this approach compared to traditional resistance training on a stable surface. Previous studies have shown that force output may be reduced with no change in muscle electromyography (EMG) activity while others have shown increased muscle EMG activity when performing resistance exercises on an unstable surface. This study compared 1RM strength, and upper body and trunk muscle EMG activity during the barbell chest press exercise on a stable (flat bench) and unstable surface (exercise ball). After familiarization, 13 subjects underwent testing for 1RM strength for the barbell chest press on both a stable bench and an exercise ball, each separated by at least 7 days. Surface EMG was recorded for 5 upper body muscles and one trunk muscle from which average root mean square of the muscle activity was calculated for the whole 1RM lift and the concentric and eccentric phases. Elbow angle during each lift was recorded to examine any range-of-motion differences between the two surfaces. The results show that there was no difference in 1RM strength or muscle EMG activity for the stable and unstable surfaces. In addition, there was no difference in elbow range-of-motion between the two surfaces. Taken together, these results indicate that there is no reduction in 1RM strength or any differences in muscle EMG activity for the barbell chest press exercise on an unstable exercise ball when compared to a stable flat surface. Moreover, these results do not support the notion that resistance exercises performed on an exercise ball are more efficacious than traditional stable exercises.     

Forging Links between Human Mental Retardation–Associated CNVs and Mouse Gene Knockout Models

Rare copy number variants (CNVs) are frequently associated with common neurological disorders such as mental retardation (MR; learning disability), autism, and schizophrenia. CNV screening in clinical practice is limited because pathological CNVs cannot be distinguished routinely from benign CNVs, and because genes underlying patients'' phenotypes remain largely unknown. Here, we present a novel, statistically robust approach that forges links between 148 MR–associated CNVs and phenotypes from ∼5,000 mouse gene knockout experiments. These CNVs were found to be significantly enriched in two classes of genes, those whose mouse orthologues, when disrupted, result in either abnormal axon or dopaminergic neuron morphologies. Additional enrichments highlighted correspondences between relevant mouse phenotypes and secondary presentations such as brain abnormality, cleft palate, and seizures. The strength of these phenotype enrichments (>100% increases) greatly exceeded molecular annotations (<30% increases) and allowed the identification of 78 genes that may contribute to MR and associated phenotypes. This study is the first to demonstrate how the power of mouse knockout data can be systematically exploited to better understand genetically heterogeneous neurological disorders.     

Identification of microRNAs associated with hyperthermia-induced cellular stress response

MicroRNAs (miRNAs) are a class of small RNAs that play a critical role in the coordination of fundamental cellular processes. Recent studies suggest that miRNAs participate in the cellular stress response (CSR), but their specific involvement remains unclear. In this study, we identify a group of thermally regulated miRNAs (TRMs) that are associated with the CSR. Using miRNA microarrays, we show that dermal fibroblasts differentially express 123 miRNAs when exposed to hyperthermia. Interestingly, only 27 of these miRNAs are annotated in the current Sanger registry. We validated the expression of the annotated miRNAs using qPCR techniques, and we found that the qPCR and microarray data was in well agreement. Computational target-prediction studies revealed that putative targets for the TRMs are heat shock proteins and Argonaute-2—the core functional unit of RNA silencing. These results indicate that cells express a specific group of miRNAs when exposed to hyperthermia, and these miRNAs may function in the regulation of the CSR. Future studies will be conducted to determine if other cells lines differentially express these miRNAs when exposed to hyperthermia.     

The good, the bad and the recovery in an assisted migration

Background

Assisted migration or translocation of species to ameliorate effects of habitat loss or changing environment is currently under scrutiny as a conservation tool. A large scale experiment of assisted migration over hundreds of kilometres was tested on a morph from a commercial fishery of southern rock lobster Jasus edwardsii, to enhance depleted populations, improve the yield and sustainability of the fishery, and test resilience to a changing climate.

Methodology and Principal Findings

Approximately 10,000 lower-valued, pale-coloured lobsters were moved from deep water to inshore sites (2 in Tasmania [TAS] and 2 in South Australia [SA]) where the high-value, red morph occurs. In TAS this was a northwards movement of 1° latitude. Growth was measured only in TAS lobsters, and reproductive status was recorded in lobsters from all locations. Pale females (TAS) grew 4 times faster than resident pale lobsters from the original site and twice as fast as red lobsters at their new location. Approximately 30% of translocated pale lobsters deferred reproduction for one year after release (SA and TAS), and grew around 1 mm yr⁻¹ less compared to translocated pale lobsters that did not defer reproduction. In spite of this stress response to translocation, females that deferred reproduction still grew 2–6 mm yr⁻¹ more than lobsters at the source site. Lobsters have isometric growth whereby volume increases as a cube of length. Consequently despite the one-year hiatus in reproduction, increased growth increases fecundity of translocated lobsters, as the increase in size provided a larger volume for producing and incubating eggs in future years.

Conclusions and Significance

Assisted migration improved egg production and growth, despite a temporary stress response, and offers a tool to improve the production, sustainability and resilience of the fishery.     

Engineering of Bacillus subtilis Strains To Allow Rapid Characterization of Heterologous Diguanylate Cyclases and Phosphodiesterases

Microbial processes, including biofilm formation, motility, and virulence, are often regulated by changes in the available concentration of cyclic dimeric guanosine monophosphate (c-di-GMP). Generally, high c-di-GMP concentrations are correlated with decreased motility and increased biofilm formation and low c-di-GMP concentrations are correlated with an increase in motility and activation of virulence pathways. The study of c-di-GMP is complicated, however, by the fact that organisms often encode dozens of redundant enzymes that synthesize and hydrolyze c-di-GMP, diguanylate cyclases (DGCs), and c-di-GMP phosphodiesterases (PDEs); thus, determining the contribution of any one particular enzyme is challenging. In an effort to develop a facile system to study c-di-GMP metabolic enzymes, we have engineered a suite of Bacillus subtilis strains to assess the effect of individual heterologously expressed proteins on c-di-GMP levels. As a proof of principle, we characterized all 37 known genes encoding predicted DGCs and PDEs in Clostridium difficile using parallel readouts of swarming motility and fluorescence from green fluorescent protein (GFP) expressed under the control of a c-di-GMP-controlled riboswitch. We found that 27 of the 37 putative C. difficile 630 c-di-GMP metabolic enzymes had either active cyclase or phosphodiesterase activity, with agreement between our motility phenotypes and fluorescence-based c-di-GMP reporter. Finally, we show that there appears to be a threshold level of c-di-GMP needed to inhibit motility in Bacillus subtilis.     

Arabidopsis NDR1 is an integrin-like protein with a role in fluid loss and plasma membrane-cell wall adhesion

Arabidopsis (Arabidopsis thaliana) NON-RACE-SPECIFIC DISEASE RESISTANCE1 (NDR1), a plasma membrane-localized protein, plays an essential role in resistance mediated by the coiled-coil-nucleotide-binding site-leucine-rich repeat class of resistance (R) proteins, which includes RESISTANCE TO PSEUDOMONAS SYRINGAE2 (RPS2), RESISTANCE TO PSEUDOMONAS SYRINGAE PV MACULICOLA1, and RPS5. Infection with Pseudomonas syringae pv tomato DC3000 expressing the bacterial effector proteins AvrRpt2, AvrB, and AvrPphB activates resistance by the aforementioned R proteins. Whereas the genetic requirement for NDR1 in plant disease resistance signaling has been detailed, our study focuses on determining a global, physiological role for NDR1. Through the use of homology modeling and structure threading, NDR1 was predicted to have a high degree of structural similarity to Arabidopsis LATE EMBRYOGENESIS ABUNDANT14, a protein implicated in abiotic stress responses. Specific protein motifs also point to a degree of homology with mammalian integrins, well-characterized proteins involved in adhesion and signaling. This structural homology led us to examine a physiological role for NDR1 in preventing fluid loss and maintaining cell integrity through plasma membrane-cell wall adhesions. Our results show a substantial alteration in induced (i.e. pathogen-inoculated) electrolyte leakage and a compromised pathogen-associated molecular pattern-triggered immune response in ndr1-1 mutant plants. As an extension of these analyses, using a combination of genetic and cell biology-based approaches, we have identified a role for NDR1 in mediating plasma membrane-cell wall adhesions. Taken together, our data point to a broad role for NDR1 both in mediating primary cellular functions in Arabidopsis through maintaining the integrity of the cell wall-plasma membrane connection and as a key signaling component of these responses during pathogen infection.     

Exome sequencing of ion channel genes reveals complex profiles confounding personal risk assessment in epilepsy

Ion channel mutations are an important cause of rare Mendelian disorders affecting brain, heart, and other tissues. We performed parallel exome sequencing of 237 channel genes in a well-characterized human sample, comparing variant profiles of unaffected individuals to those with the most common neuronal excitability disorder, sporadic idiopathic epilepsy. Rare missense variation in known Mendelian disease genes is prevalent in both groups at similar complexity, revealing that even deleterious ion channel mutations confer uncertain risk to an individual depending on the other variants with which they are combined. Our findings indicate that variant discovery via large scale sequencing efforts is only a first step in illuminating the complex allelic architecture underlying personal disease risk. We propose that in?silico modeling of channel variation in realistic cell and network models will be crucial to future strategies assessing mutation profile pathogenicity and drug response in individuals with a broad spectrum of excitability disorders.