Antarctic notothenioids dominate the fish fauna of the Southern Ocean. Evolution for millions of years at cold and stable temperatures has led to the acquisition of numerous biochemical traits that allow these fishes to thrive in sub-zero waters. The gain of antifreeze glycoproteins has afforded notothenioids the ability to avert freezing and survive at temperatures often hovering near the freezing point of seawater. Additionally, possession of cold-adapted proteins and membranes permits them to sustain appropriate metabolic rates at exceptionally low body temperatures. The notothenioid genome is also distinguished by the disappearance of traits in some species, losses that might prove costly in a warmer environment. Perhaps the best-illustrated example is the lack of expression of hemoglobin in white-blooded icefishes from the family Channichthyidae. Loss of key elements of the cellular stress response, notably the heat shock response, has also been observed. Along with their attainment of cold tolerance, notothenioids have developed an extreme stenothermy and many species perish at temperatures only a few degrees above their habitat temperatures. Thus, in light of today's rapidly changing climate, it is critical to evaluate how these extreme stenotherms will respond to rising ocean temperatures. It is conceivable that the remarkable cold specialization of notothenioids may ultimately leave them vulnerable to future thermal increases and threaten their fitness and survival. Within this context, our review provides a current summary of the biochemical losses and gains that are known for notothenioids and examines these cold-adapted traits with a focus on processes underlying thermal tolerance and acclimation capacity.

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Antarctic notothenioid fish: what are the future consequences of 'losses' and 'gains' acquired during long-term evolution at cold and stable temperatures?

This edited book contains a compilation of 14 advanced academic chapters dealing with the structure and function of membrane protein complexes. This rapidly advancing important field of study closely parallels those on soluble protein complexes, and viral protein and nucleoprotein complexes. Diverse topics are included in this book, ranging from membrane–bound enzymes to ion channels, proton pumps and photosystems. Data from X-ray crystallography, cryo-electron microscopy and other biophysical and biochemical techniques are presented throughout the book. There is extensive use of colour figures of protein structures. Throughout the book structure and function are closely correlated. The two editors, Egbert Boekema and J. Robin Harris, have worked on aspects of membrane and soluble proteins throughout their scientific careers and also have much publishing experience. The Subcellular Biochemistry series has expanded considerably in recent years, including several related volumes. The theme of protein complexes will be continued within several future volumes, thereby creating encyclopaedic coverage. The chapter topics within this book are particularly relevant to those involved in the biological and biomedical sciences. It is aimed at the advanced undergraduates, postgraduates and established researchers within this broad field. It is hoped that the book will be of interest and use to those involved with the study of cellular membranes and their associated proteins.

Membrane Protein Complexes:: Structure and Function

Isoforms of creatine kinase (CK) generate and use phosphocreatine, a concentrated and highly diffusible cellular “high energy” intermediate, for the main purpose of energy buffering and transfer in order to maintain cellular energy homeostasis. The mitochondrial CK isoform (mtCK) localizes to the mitochondrial intermembrane and cristae space, where it assembles into peripherally membrane-bound, large cuboidal homooctamers. These are part of proteolipid complexes wherein mtCK directly interacts with cardiolipin and other anionic phospholipids, as well as with the VDAC channel in the outer membrane. This leads to a stabilization and cross-linking of inner and outer mitochondrial membrane, forming so-called contact sites. Also the adenine nucleotide translocator of the inner membrane can be recruited into these proteolipid complexes, probably mediated by cardiolipin. The complexes have functions mainly in energy transfer to the cytosol and stimulation of oxidative phosphorylation, but also in restraining formation of reactive oxygen species and apoptosis. In vitro evidence indicates a putative role of mtCK in mitochondrial phospholipid distribution, and most recently a role in thermogenesis has been proposed. This review summarizes the essential structural and functional data of these mtCK complexes and describes in more detail the more recent advances in phospholipid interaction, thermogenesis, cancer and evolution of mtCK.

Mitochondrial Proteolipid Complexes of Creatine Kinase.

Studies in temperate fishes provide evidence that cardiac mitochondrial function and the capacity to fuel cardiac work contribute to thermal tolerance. Here, we tested the hypothesis that decreased cardiac aerobic metabolic capacity contributes to the lower thermal tolerance of the haemoglobinless Antarctic icefish, Chaenocephalus aceratus, compared with that of the red-blooded Antarctic species, Notothenia coriiceps. Maximal activities of citrate synthase (CS) and lactate dehydrogenase (LDH), respiration rates of isolated mitochondria, adenylate levels and changes in mitochondrial protein expression were quantified from hearts of animals held at ambient temperature or exposed to their critical thermal maximum (CTmax). Compared with C. aceratus, activity of CS, ATP concentration and energy charge were higher in hearts of N. coriiceps at ambient temperature and CTmax. While state 3 mitochondrial respiration rates were not impaired by exposure to CTmax in either species, state 4 rates, indicative of proton leakage, increased following exposure to CTmax in C. aceratus but not N. coriiceps. The interactive effect of temperature and species resulted in an increase in antioxidants and aerobic metabolic enzymes in N. coriiceps but not in C. aceratus. Together, our results support the hypothesis that the lower aerobic metabolic capacity of C. aceratus hearts contributes to its low thermal tolerance.

/pdf/cardiac-mitochondrial-metabolism-may-contribute-to-4n7lfpc9ey.pdf

Cardiac mitochondrial metabolism may contribute to differences in thermal tolerance of red- and white-blooded Antarctic notothenioid fishes.

The heart must provide its own energy requirements to sustain its continuous contractile performance and other physiological functions. This chapter provides an integrated overview of cardiac energy metabolism in fish with a particular emphasis on: maintenance of cardiac energy state; biochemical strategies for energy production; and energetic requirements to maintain contractile function, ion pumping across membranes, and protein synthesis. Major advances in our understanding of fish cardiac metabolism have come from studies of cellular ultrastructure, ion regulation, enzyme activities, select proteins involved in energy metabolism, fuel selection and energy reserves, intracellular metabolites, cardiac adaptability, and physiological performance of cardiac preparations and intact animals. Total energy expenditure of the contracting heart varies between species and includes basal and active components. The importance of myosin-bound ATP phosphatase (ATPase) for contractility, Na+/K+-ATPase for cellular ion homeostasis, and Ca2 +-ATPases for myocardial relaxation are highlighted. Fish hearts rely on well-established metabolic pathways to regenerate ATP, however, species differences are apparent. Under normoxic conditions, mitochondria produce most of the ATP used by the fish heart using aerobic metabolism and a variety of energy substrates. However, during O2-limiting conditions, anaerobic metabolism (glycolysis) becomes the major source of ATP production, despite an inherently limited capacity compared with oxidative phosphorylation. Cold temperature can also compromise several cellular processes related to cardiac energy metabolism, and yet, some fish demonstrate positive compensation of enzyme activities following cold acclimation and acclimatization. Overall, there are numerous, inter-related factors that underlie cardiac energy production and utilization.

Cardiac Energy Metabolism

Creatine kinase (CK; EC 2.7.3.2) functions as a spatial and temporal energy buffer, dampening fluctuations in ATP levels as ATP supply and demand change. There are four CK isoforms in mammals, two cytosolic isoforms (muscle [M-CK] and brain [B-CK]), and two mitochondrial isoforms (ubiquitous [uMtCK] and sarcomeric [sMtCK]). Mammalian oxidative muscle couples expression of sMtCK with M-CK, creating an energy shuttle between mitochondria and myofibrils. We hypothesized that the expression pattern and activity of CK would differ between hearts of red- and white-blooded Antarctic notothenioid fishes due to their striking differences in cardiac ultrastructure. Hearts of white-blooded icefishes (family Channichthyidae) have significantly higher mitochondrial densities compared to red-blooded species, decreasing the diffusion distance for ATP between mitochondria and myofibrils and potentially minimizing the need for CK. The distribution of CK isoforms was evaluated using western blotting and maximal activity of CK was measured in mitochondrial and cytosolic fractions and tissue homogenates of heart ventricles of red- and white-blooded notothenioids. Transcript abundance of sMtCK and M-CK was also quantified. Overall, CK activity is similar between hearts of red- and white-blooded notothenioids but hearts of icefishes lack MtCK and have higher activities of M-CK in the cytosol compared to red-blooded fishes. The absence of MtCK may compromise cardiac function under stressful conditions when ATP supply becomes limiting.

Hearts of some Antarctic fishes lack mitochondrial creatine kinase.

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Hearts of some Antarctic fishes lack mitochondrial creatine kinase.