Search

With temperatures expected to rise across the southern Rocky Mountains, the ability of native fishes to tolerate stream warming has become a critical concern for those tasked with preserving coldwater species. We used common garden experiments to evaluate the thermal tolerance of cutthroat trout ( Oncorhynchus clarkii) fry from five populations important to managers representing three sub-species. Critical thermal maxima (CTMs) were evaluated through traditional exposure trials, while optimal growth and ultimate upper incipient lethal temperatures (UUILTs) were examined over the course of 21-day trials at six static temperature treatments. Whereas CTMs differed among populations (mean = 27.91 °C, SD = 0.35 °C), UUILTs did not (mean = 24.40 °C, SD = 0.04 °C). Comparison of cubic temperature-growth functions to the traditional quadratic functions showed that adding a third-order term for temperature can improve model fit, and revealed substantial differences in optimal growth temperatures (15.4–18.3 °C). Knowledge of these thermal tolerance thresholds will help to predict the consequences of a warming climate, identify suitable habitats for repatriation, and inform water quality temperature standards established to protect these fish into the future.

Cocksfoot mottle virus (CfMV) is distributed in the Eastern and Western hemispheres. Invasiveness through introduction outside of Europe is probable.

Many vital processes in the eye are under circadian regulation, and circadian dysfunction has emerged as a potential driver of eye aging. Dietary restriction is one of the most robust lifespan-extending therapies and amplifies circadian rhythms with age. Herein, we demonstrate that dietary restriction extends lifespan in D. melanogaster by promoting circadian homeostatic processes that protect the visual system from age- and light-associated damage. Disrupting circadian rhythms in the eye by inhibiting the transcription factor, Clock (CLK), or CLK-output genes, accelerated visual senescence, induced a systemic immune response, and shortened lifespan. Flies subjected to dietary restriction were protected from the lifespan-shortening effects of photoreceptor activation. Inversely, photoreceptor inactivation, achieved via mutating rhodopsin or housing flies in constant darkness, primarily extended lifespan in flies reared on a high-nutrient diet. Our findings establish the eye as a diet-sensitive modulator of lifespan and indicate that vision is an antagonistically pleiotropic process that contributes to organismal aging.

Many vital processes in the eye are under circadian regulation, and circadian dysfunction has emerged as a potential driver of eye aging. Dietary restriction is one of the most robust lifespan-extending therapies and amplifies circadian rhythms with age. Herein, we demonstrate that dietary restriction extends lifespan in D. melanogaster by promoting circadian homoeostatic processes that protect the visual system from age- and light- associated damage. Disrupting circadian rhythms in the eye by inhibiting the transcription factor, Clock (CLK), or CLK-output genes, accelerated visual senescence, induced a systemic immune response, and shortened lifespan. Flies subjected to dietary restriction were protected from the lifespan-shortening effects of photoreceptor activation. Inversely, photoreceptor inactivation, achieved via mutating rhodopsin or housing flies in constant darkness, primarily extended lifespan in flies reared on a high-nutrient diet. Our findings establish the eye as a diet-sensitive modulator of lifespan and indicate that vision is an antagonistically pleiotropic process that contributes to organismal aging.

Little is known about the effectiveness of fishways for restoring passage to inland (nonanadromous) salmonids. We used PIT telemetry to evaluate the biological effectiveness of a vertical-slot fishway constructed to restore passage of adult Colorado River Cutthroat Trout Oncorhynchus clarkii pleuriticus (CRCT) in a small Rocky Mountain stream. Our objectives were to assess (1) fishway efficacy (whether or not the fishway restored fish passage), (2) approach efficiency (the probability that a tagged fish encountered the fishway; an index of population use), (3) attraction efficiency (the probability that a fish near the fishway located its entrance), and (4) passage efficiency (the probability that a fish entering the fishway navigated successfully through it). To account for antenna detection probabilities and avoid biases that can result from simple, proportion-based calculations, we used a variation of the Cormack–Jolly–Seber model to derive efficiency estimates. The fishway restored passage of ...

Mobile species will migrate considerable distances to find habitats suitable for meeting life history requirements, and stream‐dwelling salmonids are no exception. In April–October 2014, we used radio‐telemetry to examine habitat use and movement of 36 Colorado River cutthroat trout Oncorhynchus clarkii pleuriticus (CRCT) in a 14.9‐km fragment of Milk Creek, a relatively low‐elevation stream in the Rocky Mountains (Colorado). We also used a network of data loggers to track stream temperature across time and space. Our objectives were to (1) characterize distribution and movement of CRCT, (2) evaluate seasonal differences in distribution and movement of CRCT, and (3) explore the relationship between stream temperature and distribution and movement of CRCT. During the course of our study, median range of CRCT was 4.81 km (range = 0.14–10.94) and median total movement was 5.94 km (range = 0.14–26.02). Median location of CRCT was significantly further upstream in summer than in spring, whereas range and movement of CRCT were greater in spring than in summer. Twenty‐six of the 27 CRCT tracked through mid‐June displayed a potamodromous (freshwater migratory) life history, migrating 1.8–8.0 km upstream during the spring spawning season. Four of the seven CRCT tracked through July migrated >1.4 km in summer. CRCT selected relatively cool reaches during summer months, and early‐summer movement was positively correlated with mean stream temperature. Study fish occupied stream segments in spring and fall that were thermally unsuitable, if not lethal, to the species in summer. Although transmitter loss limited the scope of inference, our findings suggest that preferred habitat is a moving target in Milk Creek, and that CRCT move to occupy that target. Because mobile organisms move among complementary habitats and exploit seasonally‐unsuitable reaches, we recommend that spatial and temporal variability be accounted for in delineations of distributional boundaries.

In the present study we show that the master myogenic regulatory factor, MYOD1, is a positive modulator of molecular clock amplitude and functions with the core clock factors for expression of clock-controlled genes in skeletal muscle. We demonstrate that MYOD1 directly regulates the expression and circadian amplitude of the positive core clock factor Bmal1. We identify a non-canonical E-box element in Bmal1 and demonstrate that is required for full MYOD1-responsiveness. Bimolecular fluorescence complementation assays demonstrate that MYOD1 colocalizes with both BMAL1 and CLOCK throughout myonuclei. We demonstrate that MYOD1 and BMAL1:CLOCK work in a synergistic fashion through a tandem E-box to regulate the expression and amplitude of the muscle specific clock-controlled gene, Titin-cap (Tcap). In conclusion, these findings reveal mechanistic roles for the muscle specific transcription factor MYOD1 in the regulation of molecular clock amplitude as well as synergistic regulation of clock-controlled genes in skeletal muscle.

Oncorhynchus mykiss exhibits a vast array of life histories, which increases its likelihood of persistence by spreading risk of extirpation among different pathways. The Klamath River basin (California–Oregon) provides a particularly interesting backdrop for the study of life history diversity in O. mykiss, in part because the river is slated for a historic and potentially influential dam removal and habitat recolonization project. We used scale and otolith strontium isotope (87Sr/86Sr) analyses to characterize life history diversity in wild O. mykiss from the lower Klamath River basin. We also determined maternal origin (anadromous or nonanadromous) and migratory history (anadromous or nonanadromous) of O. mykiss and compared length and fecundity at age between anadromous (steelhead) and nonanadromous (Rainbow Trout) phenotypes of O. mykiss. We identified a total of 38 life history categories at maturity, which differed in duration of freshwater and ocean rearing, age at maturation, and incidence...

Key points The endogenous molecular clock in skeletal muscle is necessary for maintenance of phenotype and function. Loss of Bmal1 solely from adult skeletal muscle (iMSBmal1−/−) results in reductions in specific tension, increased oxidative fibre type and increased muscle fibrosis with no change in feeding or activity. Disruption of the molecular clock in adult skeletal muscle is sufficient to induce changes in skeletal muscle similar to those seen in the Bmal1 knockout mouse (Bmal1−/−), a model of advanced ageing. iMSBmal1−/− mice develop increased bone calcification and decreased joint collagen, which in combination with the functional changes in skeletal muscle results in altered gait. This study uncovers a fundamental role for the skeletal muscle clock in musculoskeletal homeostasis with potential implications for ageing. Abstract Disruption of circadian rhythms in humans and rodents has implicated a fundamental role for circadian rhythms in ageing and the development of many chronic diseases including diabetes, cardiovascular disease, depression and cancer. The molecular clock mechanism underlies circadian rhythms and is defined by a transcription–translation feedback loop with Bmal1 encoding a core molecular clock transcription factor. Germline Bmal1 knockout (Bmal1 KO) mice have a shortened lifespan, show features of advanced ageing and exhibit significant weakness with decreased maximum specific tension at the whole muscle and single fibre levels. We tested the role of the molecular clock in adult skeletal muscle by generating mice that allow for the inducible skeletal muscle-specific deletion of Bmal1 (iMSBmal1). Here we show that disruption of the molecular clock, specifically in adult skeletal muscle, is associated with a muscle phenotype including reductions in specific tension, increased oxidative fibre type, and increased muscle fibrosis similar to that seen in the Bmal1 KO mouse. Remarkably, the phenotype observed in the iMSBmal1−/− mice was not limited to changes in muscle. Similar to the germline Bmal1 KO mice, we observed significant bone and cartilage changes throughout the body suggesting a role for the skeletal muscle molecular clock in both the skeletal muscle niche and the systemic milieu. This emerging area of circadian rhythms and the molecular clock in skeletal muscle holds the potential to provide significant insight into intrinsic mechanisms of the maintenance of muscle quality and function as well as identifying a novel crosstalk between skeletal muscle, cartilage and bone.

We evaluated the efficacy of portable PIT detectors for tracking long-term fish movement in an open stream environment. In June and October of 2012, we PIT-tagged a total of 190 Colorado River Cutthroat Trout Oncorhynchus clarkii pleuriticus (CRCT) in a 1.7-km segment of a small, montane stream. In the summers of 2012–2013 (15 total occasions), we relocated PIT-tagged trout using portable PIT detectors. The maximum detection distance of 23-mm PIT tags ranged from 6 to 56 cm and varied with detector, detection plane, and tag orientation. Of the CRCT tagged, 38% were never detected and 43% were detected on two or more occasions. Mean detection efficiencies of PIT-tagged trout were 34% and 45% in 2012 and 2013, respectively, and were generally lower than in evaluations of closed systems and less mobile fishes. We observed a smaller range of CRCT than has been observed by others using radiotelemetry, a difference that could be explained by the spatial and temporal limitations of portable PIT detection...

Steelhead Oncorhynchus mykiss from several of the world's rivers display the half-pounder life history, a variant characterized by an amphidromous (and, less often, anadromous) return to freshwater in the year of initial ocean entry. We evaluated factors related to expression of the half-pounder life history in wild steelhead from the lower Klamath River basin, California. We also evaluated fitness consequences of the half-pounder phenotype using a simple life history model that was parameterized with our empirical data and outputs from a regional survival equation. The incidence of the half-pounder life history differed among subbasins of origin and smolt ages. Precocious maturation occurred in approximately 8% of half-pounders and was best predicted by individual length in freshwater preceding ocean entry. Adult steelhead of the half-pounder phenotype were smaller and less fecund at age than adult steelhead of the alternative (ocean contingent) phenotype. However, our data suggest that fish of t...

The endogenous molecular clock in skeletal muscle is necessary for maintenance of phenotype and function. Loss of Bmal1 solely from adult skeletal muscle (iMSBmal1(-/-) ) results in reductions in specific tension, increased oxidative fibre type and increased muscle fibrosis with no change in feeding or activity. Disruption of the molecular clock in adult skeletal muscle is sufficient to induce changes in skeletal muscle similar to those seen in the Bmal1 knockout mouse (Bmal1(-/-) ), a model of advanced ageing. iMSBmal1(-/-) mice develop increased bone calcification and decreased joint collagen, which in combination with the functional changes in skeletal muscle results in altered gait. This study uncovers a fundamental role for the skeletal muscle clock in musculoskeletal homeostasis with potential implications for ageing.Disruption of circadian rhythms in humans and rodents has implicated a fundamental role for circadian rhythms in ageing and the development of many chronic diseases including diabetes, cardiovascular disease, depression and cancer. The molecular clock mechanism underlies circadian rhythms and is defined by a transcription-translation feedback loop with Bmal1 encoding a core molecular clock transcription factor. Germline Bmal1 knockout (Bmal1 KO) mice have a shortened lifespan, show features of advanced ageing and exhibit significant weakness with decreased maximum specific tension at the whole muscle and single fibre levels. We tested the role of the molecular clock in adult skeletal muscle by generating mice that allow for the inducible skeletal muscle-specific deletion of Bmal1 (iMSBmal1). Here we show that disruption of the molecular clock, specifically in adult skeletal muscle, is associated with a muscle phenotype including reductions in specific tension, increased oxidative fibre type, and increased muscle fibrosis similar to that seen in the Bmal1 KO mouse. Remarkably, the phenotype observed in the iMSBmal1(-/-) mice was not limited to changes in muscle. Similar to the germline Bmal1 KO mice, we observed significant bone and cartilage changes throughout the body suggesting a role for the skeletal muscle molecular clock in both the skeletal muscle niche and the systemic milieu. This emerging area of circadian rhythms and the molecular clock in skeletal muscle holds the potential to provide significant insight into intrinsic mechanisms of the maintenance of muscle quality and function as well as identifying a novel crosstalk between skeletal muscle, cartilage and bone.

Diabetes is the seventh leading cause of death in the USA, and disruption of circadian rhythms is gaining recognition as a contributing factor to disease prevalence. This disease is characterized by hyperglycemia and glucose intolerance and symptoms caused by failure to produce and/or respond to insulin. The skeletal muscle is a key insulin-sensitive metabolic tissue, taking up ~80 % of postprandial glucose. To address the role of the skeletal muscle molecular clock to insulin sensitivity and glucose tolerance, we generated an inducible skeletal muscle-specific Bmal1 −/− mouse (iMSBmal1 −/−). Progressive changes in body composition (decreases in percent fat) were seen in the iMSBmal1 −/− mice from 3 to 12 weeks post-treatment as well as glucose intolerance and non-fasting hyperglycemia. Ex vivo analysis of glucose uptake revealed that the extensor digitorum longus (EDL) muscles did not respond to either insulin or 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) stimulation. RT-PCR and Western blot analyses demonstrated a significant decrease in mRNA expression and protein content of the muscle glucose transporter (Glut4). We also found that both mRNA expression and activity of two key rate-limiting enzymes of glycolysis, hexokinase 2 (Hk2) and phosphofructokinase 1 (Pfk1), were significantly reduced in the iMSBmal1 −/− muscle. Lastly, results from metabolomics analyses provided evidence of decreased glycolytic flux and uncovered decreases in some tricarboxylic acid (TCA) intermediates with increases in amino acid levels in the iMSBmal1 −/− muscle. These findings suggest that the muscle is relying predominantly on fat as a fuel with increased protein breakdown to support the TCA cycle. These data support a fundamental role for Bmal1, the endogenous circadian clock, in glucose metabolism in the skeletal muscle. Our findings have implicated altered molecular clock dictating significant changes in altered substrate metabolism in the absence of feeding or activity changes. The changes in body composition in our model also highlight the important role that changes in skeletal muscle carbohydrate, and fat metabolism can play in systemic metabolism.

Collagen VI myopathies are genetic disorders caused by mutations in collagen 6 A1, A2 and A3 genes, ranging from the severe Ullrich congenital muscular dystrophy to the milder Bethlem myopathy, which is recapitulated by collagen-VI-null (Col6a1(-/-)) mice. Abnormalities in mitochondria and autophagic pathway have been proposed as pathogenic causes of collagen VI myopathies, but the link between collagen VI defects and these metabolic circuits remains unknown. To unravel the expression profiling perturbation in muscles with collagen VI myopathies, we performed a deep RNA profiling in both Col6a1(-/-)mice and patients with collagen VI pathology. The interactome map identified common pathways suggesting a previously undetected connection between circadian genes and collagen VI pathology. Intriguingly, Bmal1(-/-)(also known as Arntl) mice, a well-characterized model displaying arrhythmic circadian rhythms, showed profound deregulation of the collagen VI pathway and of autophagy-related genes. The involvement of circadian rhythms in collagen VI myopathies is new and links autophagy and mitochondrial abnormalities. It also opens new avenues for therapies of hereditary myopathies to modulate the molecular clock or potential gene-environment interactions that might modify muscle damage pathogenesis.

Skeletal muscle is a major contributor to whole-body metabolism as it serves as a depot for both glucose and amino acids, and is a highly metabolically active tissue. Within skeletal muscle exists an intrinsic molecular clock mechanism that regulates the timing of physiological processes. A key function of the clock is to regulate the timing of metabolic processes to anticipate time of day changes in environmental conditions. The purpose of this study was to identify metabolic genes that are expressed in a circadian manner and determine if these genes are regulated downstream of the intrinsic molecular clock by assaying gene expression in an inducible skeletal muscle-specific Bmal1 knockout mouse model (iMS-Bmal1 −/− ). We used circadian statistics to analyze a publicly available, high-resolution time-course skeletal muscle expression dataset. Gene ontology analysis was utilized to identify enriched biological processes in the skeletal muscle circadian transcriptome. We generated a tamoxifen-inducible skeletal muscle-specific Bmal1 knockout mouse model and performed a time-course microarray experiment to identify gene expression changes downstream of the molecular clock. Wheel activity monitoring was used to assess circadian behavioral rhythms in iMS-Bmal1 −/− and control iMS-Bmal1 +/+ mice. The skeletal muscle circadian transcriptome was highly enriched for metabolic processes. Acrophase analysis of circadian metabolic genes revealed a temporal separation of genes involved in substrate utilization and storage over a 24-h period. A number of circadian metabolic genes were differentially expressed in the skeletal muscle of the iMS-Bmal1 −/− mice. The iMS-Bmal1 −/− mice displayed circadian behavioral rhythms indistinguishable from iMS-Bmal1 +/+ mice. We also observed a gene signature indicative of a fast to slow fiber-type shift and a more oxidative skeletal muscle in the iMS-Bmal1 −/− model. These data provide evidence that the intrinsic molecular clock in skeletal muscle temporally regulates genes involved in the utilization and storage of substrates independent of circadian activity. Disruption of this mechanism caused by phase shifts (that is, social jetlag) or night eating may ultimately diminish skeletal muscle’s ability to efficiently maintain metabolic homeostasis over a 24-h period.

All employee benefit plans are potential targets of fraudulent schemes. Smaller plans are targeted by unscrupulous brokers and promoters selling fraudulent policies; plans large enough to be self-insured face greater risks of fraud by providers and participants misrepresenting claims. Plan trustees, administrators and consultants should be alert to the many ways fraudulent schemes manifest themselves and to the legal remedies available; establish investigative programs to detect and discourage fraud; and promote education and plan incentives for participants to report fraud.

The geological results of a borehole drilled to investigate the coincidence of centres of a zonal pattern of mineralization (Dunham 1934) with areas of strong negative Bouguer anomaly are presented. The presence of a granite batholith with cupolas, postulated by Bott & Masson-Smith (1957) has been proved; the top surface of the granite was found at 1281ft depth and the boring was continued to 2650 ft in granite. The section begins in the Great Limestone at the base of the Namurian; a normal succession in the Middle Limestone Group (Lower Carboniferous) is revealed, the Smiddy Limestone with Girvanella Band being reached at 1056 ft 6in. The Lower Limestone Group differs from the section in Teesdale and the Pennine escarpment; in particular, beds equivalent to the Melmerby Scar Limestone, identified by their fauna of algae, corals, and brachiopods, have a rubbly lithology and are split by bands of seatearth, sandstone, and shale. Beneath them, clastic sediments 38 ft thick with marine fossils rest on the weathered surface of the granite. Two quartz-dolerite sheets were proved; the Little Whin sill, 6ft, is in the Three Yard Limestone as at Stanhope, while the Great Whin sill, 192ft 9in, lies beneath the Jew Limestone, stratigraphically lower than in Upper Weardale. The Weardale granite, carrying biotite and abundant muscovite, has a low-dipping foliation in the upper part, but this becomes less obvious below 2225ft depth. Preliminary X-ray studies indicate that low albite, orthoclase, maximum microcline, and forms intermediate between the last two are present. Analyses of representative rocks for major and trace elements are given. Xenoliths are conspicuously absent, but aplites and pegmatites are common. The mineralogical and chemical effects of weathering before Carboniferous sedimentation, and of the mineralization, are described. The borehole was sited near the crossing of the Boltsburn lead vein (ene-wsw) and the Red fluorite-iron vein (ese-wnw), both of which dip towards it. Strong metasomatic mineralization, including green fluorite, blende, and quartz occurs in the Tynebottom, Jew, and Lower Little limestones. Numerous small veins were also cut both in the sediments and the granite. Though chalcopyrite is present against the lower sediments, there is no evidence of a concentrated copper zone. Fluorite continues into the granite, and pyrrhotine, not present above, is found from 1355 ft depth. Mineralization continues to much greater depths than have previously been proved in the area; its source presumably lies beneath the granite cupolas, which may, however, have guided the rising fluids.