Abstract
The ability of an animal, normally dependent on aerobic respiration, to suspend breathing and enter an anoxic state for long term survival is clearly a fascinating feat, and has been the focus of numerous biochemical studies. When anoxia tolerant turtles are faced with periods of oxygen deprivation, numerous physiological and biochemical alterations take place in order to facilitate vital reductions in ATP consumption. Such strategies include reversible post-translational modifications as well as the implementation of translation and transcription controls facilitating metabolic depression. Although it is clear that anoxic survival relies on the suppression of ATP consuming processes, the state of the cell cycle in anoxia tolerant vertebrates remain elusive. Several anoxia tolerant invertebrate and embryonic vertebrate models display cell cycle arrest when presented with anoxic stress. Despite this, the cell cycle has not yet been characterized for anoxia tolerant turtles. Understanding how vertebrates respond to anoxia can have important clinical implications. Uncontrollable cellular proliferation and hypoxic tumor progression are inescapably linked in vertebrate tissues. Consequentially, the molecular mechanisms controlling these processes have profound clinical consequences. This review article will discuss the theory of cell cycle arrest in anoxic vertebrates and more specifically, the control of the retinoblastoma pathway, the molecular markers of cell cycle arrest, the activation of checkpoint kinases, and the possibility of translational controls implemented by microRNAs.
Keywords: Cell cycle, microRNA, anoxia tolerance, retinoblastoma, ischemia, chromatin remodeling, Trachemys scripta elegans
Current Genomics
Title: Perspectives in Cell Cycle Regulation: Lessons from an Anoxic Vertebrate
Volume: 10 Issue: 8
Author(s): Kyle K. Biggar and Kenneth B. Storey
Affiliation:
Keywords: Cell cycle, microRNA, anoxia tolerance, retinoblastoma, ischemia, chromatin remodeling, Trachemys scripta elegans
Abstract: The ability of an animal, normally dependent on aerobic respiration, to suspend breathing and enter an anoxic state for long term survival is clearly a fascinating feat, and has been the focus of numerous biochemical studies. When anoxia tolerant turtles are faced with periods of oxygen deprivation, numerous physiological and biochemical alterations take place in order to facilitate vital reductions in ATP consumption. Such strategies include reversible post-translational modifications as well as the implementation of translation and transcription controls facilitating metabolic depression. Although it is clear that anoxic survival relies on the suppression of ATP consuming processes, the state of the cell cycle in anoxia tolerant vertebrates remain elusive. Several anoxia tolerant invertebrate and embryonic vertebrate models display cell cycle arrest when presented with anoxic stress. Despite this, the cell cycle has not yet been characterized for anoxia tolerant turtles. Understanding how vertebrates respond to anoxia can have important clinical implications. Uncontrollable cellular proliferation and hypoxic tumor progression are inescapably linked in vertebrate tissues. Consequentially, the molecular mechanisms controlling these processes have profound clinical consequences. This review article will discuss the theory of cell cycle arrest in anoxic vertebrates and more specifically, the control of the retinoblastoma pathway, the molecular markers of cell cycle arrest, the activation of checkpoint kinases, and the possibility of translational controls implemented by microRNAs.
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Cite this article as:
Biggar K. Kyle and Storey B. Kenneth, Perspectives in Cell Cycle Regulation: Lessons from an Anoxic Vertebrate, Current Genomics 2009; 10 (8) . https://dx.doi.org/10.2174/138920209789503905
DOI https://dx.doi.org/10.2174/138920209789503905 |
Print ISSN 1389-2029 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5488 |
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