Abstract
Polymerization of actin filaments and microtubules constitutes a ubiquitous demand for cellular adenosine-5′-triphosphate (ATP) and guanosine-5′-triphosphate (GTP). In anoxia-tolerant animals, ATP consumption is minimized during overwintering conditions, but little is known about the role of cell structure in anoxia tolerance. Studies of overwintering mammals have revealed that microtubule stability in neurites is reduced at low temperature, resulting in withdrawal of neurites and reduced abundance of excitatory synapses. Literature for turtles is consistent with a similar downregulation of peripheral cytoskeletal activity in brain and liver during anoxic overwintering. Downregulation of actin dynamics, as well as modification to microtubule organization, may play vital roles in facilitating anoxia tolerance. Mitochondrial calcium release occurs during anoxia in turtle neurons, and subsequent activation of calcium-binding proteins likely regulates cytoskeletal stability. Production of reactive oxygen species (ROS) formation can lead to catastrophic cytoskeletal damage during overwintering and ROS production can be regulated by the dynamics of mitochondrial interconnectivity. Therefore, suppression of ROS formation is likely an important aspect of cytoskeletal arrest. Furthermore, gasotransmitters can regulate ROS levels, as well as cytoskeletal contractility and rearrangement. In this review we will explore the energetic costs of cytoskeletal activity, the cellular mechanisms regulating it, and the potential for cytoskeletal arrest being an important mechanism permitting long-term anoxia survival in anoxia-tolerant species, such as the western painted turtle and goldfish.
Highlights
This was the first study to examine tau regulation in non-mammalian overwintering and raised the possibility that cytoskeletal inhibition mediated by microtubule associated protein (MAP) is a widespread adaptation to metabolic rate depression, at least in neurons, begging the question as to whether such adaptations extend to anoxia tolerance among animals
We have presented an argument for a contribution of cytoskeletal structure to metabolic rate depression in anoxic animals, such as turtles and goldfish, which we refer to as “Cytoskeletal Arrest” (Figure 4)
In combining the idea of Bickler and Buck [10,155], that calcium-mediated actin depolymerization can contribute to metabolic rate depression, and the model constructed by Hawrysh and Buck [161], wherein mitochondria regulate anoxic calcium release, we propose a possible means of linking cytoskeletal structure to mitochondrial environmental sensing
Summary
Since the endosymbiotic origin of mitochondria [1], oxygen availability has been essential to eukaryote life, but animal species have repeatedly evolved to occupy niches that experience periods where oxygen availability is low (hypoxia), or absent entirely (anoxia; [2]). The western painted turtle Chrysemys picta belli was determined to be the most anoxia-tolerant vertebrate tetrapod. This is likely the result of its northern overwintering range, which necessitates the ability to survive under ice-covered lakes and ponds for up to four months [5,6]. Proposed isolated turtle hepatocytes as a model anoxia-tolerant primary cell system due to the relative homogeneity of cell type and size, large glycogen reserves, and role in whole animal anoxic metabolism. No studies have investigated the role of underlying structural processes in reducing anoxic ATP demand, and the phenotype of overwintering turtle cells remains unexplored. We have especially drawn on anoxia tolerance of the western painted turtle (painted turtle) and the more readily and widely studied red-eared slider (red-eared turtle) and have included implications for mitochondrial function
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