Combining ocean predictions with physiological understanding yields the ability to forecast habitat multiple years into the future for a wide variety of marine organisms. However, several challenges ...remain before we see the regular production and use of marine habitat forecasts.
A surprising result from the analysis of data for fish populations in Europe and North America could change ways of thinking about the ecological consequences of such events. Furthermore, this work ...focuses solely on fish species that are caught on or close to the bottom of continental shelves (sites located near land and less than 500 metres deep). The effects of heatwaves have been reported for many other groups of organisms, including coral reefs, kelp forests, surface-dwelling (pelagic) fish, marine mammals, seabirds and species that dwell in the sea bed (benthic species)6.
The mechanisms initiating protein acylation in mitochondria are unknown.
Results: The pH and acyl-CoA concentrations of the mitochondrial matrix are sufficient to cause protein lysine acetylation and ...succinylation.
Conclusion: Protein acylation in mitochondria may be a nonenzymatic event facilitated by the alkaline pH and high acyl-CoA concentrations.
Significance: The mitochondrial deacylases SIRT3 and SIRT5 may have evolved to regulate nonenzymatic protein acylation.
Alterations in mitochondrial protein acetylation are implicated in the pathophysiology of diabetes, the metabolic syndrome, mitochondrial disorders, and cancer. However, a viable mechanism responsible for the widespread acetylation in mitochondria remains unknown. Here, we demonstrate that the physiologic pH and acyl-CoA concentrations of the mitochondrial matrix are sufficient to cause dose- and time-dependent, but enzyme-independent acetylation and succinylation of mitochondrial and nonmitochondrial proteins in vitro. These data suggest that protein acylation in mitochondria may be a chemical event facilitated by the alkaline pH and high concentrations of reactive acyl-CoAs present in the mitochondrial matrix. Although these results do not exclude the possibility of enzyme-mediated protein acylation in mitochondria, they demonstrate that such a mechanism may not be required in its unique chemical environment. These findings may have implications for the evolutionary roles that the mitochondria-localized SIRT3 deacetylase and SIRT5 desuccinylase have in the maintenance of metabolic health.
There is an intimate interplay between cellular metabolism and the pathophysiology of disease. Mitochondria are essential to maintaining and regulating metabolic function of cells and organs. ...Mitochondrial dysfunction is implicated in diverse diseases, such as cardiovascular disease, diabetes and metabolic syndrome, neurodegeneration, cancer, and aging. Multiple reversible post-translational protein modifications are located in the mitochondria that are responsive to nutrient availability and redox conditions, and which can act in protein–protein interactions to modify diverse mitochondrial functions. Included in this are physiologic redox signaling via reactive oxygen and nitrogen species, phosphorylation, O-GlcNAcylation, acetylation, and succinylation, among others. With the advent of mass proteomic screening techniques, there has been a vast increase in the array of known mitochondrial post-translational modifications and their protein targets. The functional significance of these processes in disease etiology, and the pathologic response to their disruption, are still under investigation. However, many of these reversible modifications act as regulatory mechanisms in mitochondria and show promise for mitochondrial-targeted therapeutic strategies. This review addresses the current knowledge of post-translational processing and signaling mechanisms in mitochondria, and their implications in health and disease.
Functional traits, rather than taxonomic identity, determine the fitness of individuals in their environment: traits of marine organisms are therefore expected to vary across the global ocean as a ...function of the environment. Here, we quantify such spatial and seasonal variations based on extensive empirical data and present the first global biogeography of key traits (body size, feeding mode, relative offspring size and myelination) for pelagic copepods, the major group of marine zooplankton. We identify strong patterns with latitude, season and between ocean basins that are partially (c. 50%) explained by key environmental drivers. Body size, for example decreases with temperature, confirming the temperature‐size rule, but surprisingly also with productivity, possibly driven by food‐chain length and size‐selective predation. Patterns unrelated to environmental predictors may originate from phylogenetic clustering. Our maps can be used as a test‐bed for trait‐based mechanistic models and to inspire next‐generation biogeochemical models.
The advent of user-friendly satellite-based measurements of daily sea surface temperatures provided the necessary data, and exponential increases in computational power and storage removed practical ...barriers to analysing these big data sets. In some regions, cooler water might be only a few kilometres away - such as areas near frontal zones (the interfaces of distinct hydrological regions of the ocean), or near upwelling zones (where cold, deep waters are brought to the surface). ...the habitat of a marine organism is shaped not only by temperature, but also by factors such as water depth, proximity to the coastline and the nature of the sea bed. ...finding and reaching a suitable alternative habitat takes time, which means that species displacements expected on the basis of the thermal-displacement metric might not always occur, especially for short-duration MHWs.
Abstract
Forecasting variation in the recruitment to fish stocks is one of the most challenging and long-running problems in fisheries science and essentially remains unsolved today. Traditionally, ...recruitment forecasts are developed and evaluated based on explanatory and goodness-of-fit approaches that do not reflect their ability to predict beyond the data on which they were developed. Here, we propose a new generic framework that allows the skill and value of recruitment forecasts to be assessed in a manner that is relevant to their potential use in an operational setting. We assess forecast skill based on predictive power using a retrospective forecasting approach inspired by meteorology, and emphasize the importance of assessing these forecasts relative to a baseline. We quantify the value of these forecasts using an economic cost-loss decision model that is directly relevant to many forecast users. We demonstrate this framework using four stocks of lesser sandeel (Ammodytes marinus) in the North Sea, showing for the first time in an operationally realistic setting that skilful and valuable forecasts are feasible in two of these areas. This result shows the ability to produce valuable short-term recruitment forecasts, and highlights the need to revisit our approach to and understanding of recruitment forecasting.
With the majority of the global human population living in coastal regions, correctly characterizing the climate risk that ocean-dependent communities and businesses are exposed to is key to ...prioritizing the finite resources available to support adaptation. We apply a climate risk analysis across the European fisheries sector to identify the most at-risk fishing fleets and coastal regions and then link the two analyses together. We employ an approach combining biological traits with physiological metrics to differentiate climate hazards between 556 populations of fish and use these to assess the relative climate risk for 380 fishing fleets and 105 coastal regions in Europe. Countries in southeast Europe as well as the United Kingdom have the highest risks to both fishing fleets and coastal regions overall, while in other countries, the risk-profile is greater at either the fleet level or at the regional level. European fisheries face a diversity of challenges posed by climate change; climate adaptation, therefore, needs to be tailored to each country, region, and fleet's specific situation. Our analysis supports this process by highlighting where and what adaptation measures might be needed and informing where policy and business responses could have the greatest impact.
The childhood heart disease of Friedreich's Ataxia (FRDA) is characterized by hypertrophy and failure. It is caused by loss of frataxin (FXN), a mitochondrial protein involved in energy homeostasis. ...FRDA model hearts have increased mitochondrial protein acetylation and impaired sirtuin 3 (SIRT3) deacetylase activity. Protein acetylation is an important regulator of cardiac metabolism and loss of SIRT3 increases susceptibility of the heart to stress-induced cardiac hypertrophy and ischemic injury. The underlying pathophysiology of heart failure in FRDA is unclear. The purpose of this study was to examine in detail the physiologic and acetylation changes of the heart that occur over time in a model of FRDA heart failure. We predicted that increased mitochondrial protein acetylation would be associated with a decrease in heart function in a model of FRDA.
A conditional mouse model of FRDA cardiomyopathy with ablation of FXN (FXN KO) in the heart was compared to healthy controls at postnatal days 30, 45 and 65. We evaluated hearts using echocardiography, cardiac catheterization, histology, protein acetylation and expression.
Acetylation was temporally progressive and paralleled evolution of heart failure in the FXN KO model. Increased acetylation preceded detectable abnormalities in cardiac function and progressed rapidly with age in the FXN KO mouse. Acetylation was also associated with cardiac fibrosis, mitochondrial damage, impaired fat metabolism, and diastolic and systolic dysfunction leading to heart failure. There was a strong inverse correlation between level of protein acetylation and heart function.
These results demonstrate a close relationship between mitochondrial protein acetylation, physiologic dysfunction and metabolic disruption in FRDA hypertrophic cardiomyopathy and suggest that abnormal acetylation contributes to the pathophysiology of heart disease in FRDA. Mitochondrial protein acetylation may represent a therapeutic target for early intervention.
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