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First published online May 8, 2007
Journal of Experimental Biology 210, 1700-1714 (2007)
Published by The Company of Biologists 2007
doi: 10.1242/jeb.02716

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Review Article

Tribute to P. L. Lutz: putting life on `pause' – molecular regulation of hypometabolism

Kenneth B. Storey^* and Janet M. Storey

Institute of Biochemistry, Carleton University, 1125 Colonel By Drive, Ottawa, Ontario, K1S 5B6, Canada

^* Author for correspondence (e-mail: kenneth_storey{at}carleton.ca)

Accepted 15 January 2007

Entry into a hypometabolic state is an important survival strategy for many organisms when challenged by environmental stress, including low oxygen, cold temperatures and lack of food or water. The molecular mechanisms that regulate transitions to and from hypometabolic states, and stabilize long-term viability during dormancy, are proving to be highly conserved across phylogenic lines. A number of these mechanisms were identified and explored using anoxia-tolerant turtles as the model system, particularly from the research contributions made by Dr Peter L. Lutz in his explorations of the mechanisms of neuronal suppression in anoxic brain. Here we review some recent advances in understanding the biochemical mechanisms of metabolic arrest with a focus on ideas such as the strategies used to reorganize metabolic priorities for ATP expenditure, molecular controls that suppress cell functions (e.g. ion pumping, transcription, translation, cell cycle arrest), changes in gene expression that support hypometabolism, and enhancement of defense mechanisms (e.g. antioxidants, chaperone proteins, protease inhibitors) that stabilize macromolecules and promote long-term viability in the hypometabolic state.

Key words: metabolic rate depression, anoxia tolerance, hibernation, reversible protein phosphorylation, signal transduction, stress-induced gene expression, cell cycle arrest, antioxidant defense

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A TRIBUTE TO PETER LUTZ

Laura Blackburn
JEB 2007 210: i. [Full Text]  

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